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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
A1cfTg(Myh6-cre/Esr1*)1Jmk
transgene insertion 1, Jeffery D Molkentin
MGI:3050453
Summary 37 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Cd36tm2.1Mfe/Cd36tm2.1Mfe
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
B6.Cg-Cd36tm2.1Mfe A1cfTg(Myh6-cre/Esr1*)1Jmk MGI:5755142
cn2
Mybpc3tm2.1Rmos/Mybpc3tm2.1Rmos
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129 * C57BL/6 * FVB/N MGI:5523783
cn3
Srftm1Zli/Srftm1Zli
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129 * C57BL/6J * FVB/N MGI:5575856
cn4
Mcattm1.1Ssmi/Mcattm1.1Ssmi
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N MGI:5466537
cn5
Atp2a2tm1.1Iemr/Atp2a2tm1.1Iemr
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129P2/OlaHsd * C57BL/6J * FVB/N MGI:4441305
cn6
Ldb3tm4Chen/Ldb3tm4Chen
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129S1/Sv * 129X1/SvJ * Black Swiss * FVB/N MGI:3832390
cn7
Ryr2tm1Krbr/Ryr2tm1Krbr
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N MGI:5576935
cn8
Cacna1ctm3Hfm/Cacna1ctm4Hfm
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N MGI:5291995
cn9
Ryr2tm1Krbr/Ryr2tm3.1Swch
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129S1/Sv * 129X1/SvJ * FVB/N MGI:5606049
cn10
Cacna1ctm1Ggm/Cacna1ctm1Ggm
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129S1/Sv * 129X1/SvJ * FVB/N MGI:5446618
cn11
Ptentm1Hwu/Ptentm1Hwu
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129S4/SvJae * FVB/N MGI:4882047
cn12
Txniptm1Rlee/Txniptm1Rlee
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129S4/SvJae * FVB/N MGI:3818746
cn13
Mcutm1.1Jmol/Mcutm1.1Jmol
A1cfTg(Myh6-cre/Esr1*)1Jmk/A1cf+
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6J * FVB/N MGI:5779906
cn14
Pik3cbtm1.1Rzl/Pik3cbtm1.1Rzl
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129S4/SvJaeSor * C57BL/6 * FVB/N MGI:4845868
cn15
Pik3catm1.1Rzl/Pik3catm1.1Rzl
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129S4/SvJaeSor * C57BL/6 * FVB/N MGI:4845867
cn16
Cdh2tm1Glr/Cdh2Gt(OST49160)Lex
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129S5/SvEvBrd * 129S6/SvEvTac * C57BL/6J * FVB/N MGI:3580161
cn17
Plce1tm2Avsm/Plce1tm2Avsm
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129S6/SvEvTac * C57BL/6 * FVB/N MGI:5514169
cn18
Tgfbr2tm1.2Hlm/Tgfbr2tm1.2Hlm
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129S6/SvEvTac * C57BL/6 * FVB/N MGI:5523280
cn19
Juptm1.1Glr/Juptm1.1Glr
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129S6/SvEvTac * C57BL/6 * FVB/N * SJL MGI:4947241
cn20
Wdr1tm1.1Zzy/Wdr1tm1.1Zzy
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129S6/SvEvTac * C57BL/6J MGI:5688487
cn21
Cdh2tm1Glr/Cdh2tm1Hyn
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129S6/SvEvTac * C57BL/6J * FVB/N MGI:3580162
cn22
Tgfbr1tm1.1Karl/Tgfbr1tm1.1Karl
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129S/Sv * C57BL/6 * FVB/N MGI:5523277
cn23
Hcn4tm1.1Ggc/Hcn4tm1.1Ggc
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129S/SvEv * C57BL/6 * FVB/N MGI:4888970
cn24
Atg5tm1Myok/Atg5tm1Myok
A1cfTg(Myh6-cre/Esr1*)1Jmk/?
involves: 129S/SvEv * FVB/N MGI:3713115
cn25
Ptgs2tm1Gaf/Ptgs2tm1Gaf
A1cfTg(Myh6-cre/Esr1*)1Jmk/?
involves: 129/Sv * C57BL/6 * FVB/N MGI:3844714
cn26
Ctnna1tm1Efu/Ctnna1tm1Efu
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: 129X1/SvJ * FVB/N MGI:5504499
cn27
Dmdtm1.1Know/Dmdtm1.1Know
Tg(Myh6-2A)#Know/0
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: BALB/c * C3H * C57BL/6 * FVB/N MGI:5569640
cn28
Tnni3ktm1Tfo/Tnni3ktm1Tfo
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: C57BL/6 * FVB/N MGI:5614265
cn29
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Tspotm1.1Maf/Tspotm1.1Maf
involves: C57BL/6 * FVB/N MGI:5588664
cn30
Akap6tm1.1Mskf/Akap6tm1.1Mskf
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: C57BL/6 * FVB/N * SJL MGI:5603568
cn31
Tg(CAG-DMPK*)1323Coop/0
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: FVB MGI:5426794
cn32
Irx3tm3Hui/Irx3tm3Hui
Irx5tm3Hui/Irx5tm3Hui
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: FVB MGI:5444495
cn33
Abcb8tm1Hard/Abcb8tm1Hard
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: FVB MGI:5315861
cn34
Cxadrtm1Mgot/Cxadrtm1Mgot
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: FVB MGI:3812384
cn35
Senp2tm1.1Eyeh/Senp2tm1.1Eyeh
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: FVB/N MGI:5750664
cn36
Hif1atm1Stom/Hif1atm1Stom
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
involves: FVB/N MGI:3815316
ot37
A1cfTg(Myh6-cre/Esr1*)1Jmk/0 involves: 129S/Sv * C57BL/6 * FVB/N MGI:5523279


Genotype
MGI:5755142
cn1
Allelic
Composition
Cd36tm2.1Mfe/Cd36tm2.1Mfe
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
B6.Cg-Cd36tm2.1Mfe A1cfTg(Myh6-cre/Esr1*)1Jmk
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Cd36tm2.1Mfe mutation (0 available); any Cd36 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• following ischemia/reperfusion, ex vivo perfused working hearts from tamoxifen-treated mice display significantly improved myocardial functional recovery relative to control hearts, as shown by increased heart rate peak systolic pressure (HR PSP) and cardiac power compared to the pre-ischemic phase
• improved recovery is associated with lower calculated proton production prior to and following ischemia relative to control hearts
• during reperfusion, ATP production relative to cardiac work is dramatically reduced and myocardial lactate levels are significantly decreased, indicating increased post-ischemic cardiac efficiency relative to control hearts
• at 4-6 weeks after tamoxifen treatment, ex vivo perfused working hearts show a 48% reduction in FA (palmitate) oxidation rates relative to control hearts
• at 4-6 weeks after tamoxifen treatment, ex vivo perfused working hearts show a 68% increase in glucose oxidation rates, with no significant change in glycolytic rates relative to control hearts
• despite switch to increased mitochondrial oxidation of glucose versus FAs (53% of TCA cycle acetyl-CoA production versus 26% in controls), total TCA cycle acetyl-CoA production and total ATP production via exogenously supplied substrates are not significantly altered
• at 4-6 weeks after tamoxifen treatment, ex vivo perfused working hearts display significantly decreased fatty acid (palmitate) uptake relative to control hearts
• however, serum concentrations of free FAs are not significantly altered
• at 4-6 weeks after tamoxifen treatment, ex vivo perfused working hearts show a significant reduction in myocardial triacylglycerol (TAG) content relative to control hearts

cardiovascular system
N
• at 4-6 weeks after tamoxifen treatment, H&E staining showed normal cardiomyocyte morphology in apical heart sections
• ex vivo perfused working hearts show normal heart rate (HR), HR peak systolic pressure (PSP), cardiac power, cardiac output and coronary flow rates, as well as normal myocardial ATP, ADP, AMP, and phosphocreatine levels during aerobic perfusions
• in vivo, tamoxifen-treated hearts show normal baseline cardiac function with no detectable structural or morphological abnormalities
• following ischemia/reperfusion, ex vivo perfused working hearts from tamoxifen-treated mice display significantly improved myocardial functional recovery relative to control hearts, as shown by increased heart rate peak systolic pressure (HR PSP) and cardiac power compared to the pre-ischemic phase
• improved recovery is associated with lower calculated proton production prior to and following ischemia relative to control hearts
• during reperfusion, ATP production relative to cardiac work is dramatically reduced and myocardial lactate levels are significantly decreased, indicating increased post-ischemic cardiac efficiency relative to control hearts

cellular
• at 4-6 weeks after tamoxifen treatment, ex vivo perfused working hearts show a 48% reduction in FA (palmitate) oxidation rates relative to control hearts




Genotype
MGI:5523783
cn2
Allelic
Composition
Mybpc3tm2.1Rmos/Mybpc3tm2.1Rmos
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129 * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Mybpc3tm2.1Rmos mutation (0 available); any Mybpc3 mutation (15 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• gross cardiac morphology is normal 8 weeks after tamoxifen treatment
• myocyte disarray in tamoxifen-treated mice 12 weeks after transaortic constriction
• at 20 weeks in tamoxifen-treated mice
• increased posterior wall thickness in diastole after 20 weeks of tamoxifen treatment
• increased left ventricle internal dimension in tamoxifen-treated mice after transaortic constriction
• however, internal dimension is normal after 20 weeks of tamoxifen treatment
• in tamoxifen-treated mice 12 weeks after transaortic constriction
• highly variable focal and diffuse 20 weeks after tamoxifen treatment
• decreased ejection fraction and isovolumic relaxation time in tamoxifen-treated mice
• reduced fractional shortening in tamoxifen-treated mice after transaortic constriction
• however, tamoxifen-treated mice exhibit normal left ventricle posterior wall thickness and left ventricle internal diameter
• following transaortic constriction, tamoxifen-treated mice exhibit increased left ventricle internal dimension and reduced fractional shortening compared with control mice

homeostasis/metabolism
• following transaortic constriction, tamoxifen-treated mice exhibit increased left ventricle internal dimension and reduced fractional shortening compared with control mice

muscle
• myocyte disarray in tamoxifen-treated mice 12 weeks after transaortic constriction
• at 20 weeks in tamoxifen-treated mice
• decreased ejection fraction and isovolumic relaxation time in tamoxifen-treated mice
• reduced fractional shortening in tamoxifen-treated mice after transaortic constriction
• however, tamoxifen-treated mice exhibit normal left ventricle posterior wall thickness and left ventricle internal diameter




Genotype
MGI:5575856
cn3
Allelic
Composition
Srftm1Zli/Srftm1Zli
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129 * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Srftm1Zli mutation (0 available); any Srf mutation (11 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice die 8 to 10 weeks after tamoxifen injection due to rapid progression to heart failure; mice appear sick and become inactive a few days before death

cardiovascular system
• following tamoxifen treatment, hearts show an irregular alignment of cardiomyocytes, with frequent gaps between cells
• amount of polymerized F-actin in cardiomyocytes progressively decreases after tamoxifen treatment
• myofibrils at the intercalated disks are often stretched and fragmented following tamoxifen treatment
• Z disks of cardiomyocytes are misaligned and myofibrils are split 60 days after tamoxifen treatment
• 60 days after tamoxifen treatment, cardiac tissue shows a lower density of myofibrils and a defect in demarcation of Z lines and M lines
• 95% of intercalated disks of hearts are enlarged, irregularly shaped, and are thicker 60 days after tamoxifen treatment
• intercalated disks show extensive interdigitation and the presence of lacunae, a widened space at the site of myofibril attachment to the intercalated disks, following tamoxifen treatment
• hearts show features of eccentric hypertrophy 2 months after tamoxifen treatment, with dilation of the ventricular chambers
• however, no concentric hypertrophy is seen
• mild left ventricle enlargement is seen 1 month after tamoxifen treatment, without significant left atrium remodeling and moderately increased left ventricle mass index
• dilation of the ventricular chambers is seen 2 months after tamoxifen treatment
• mild fibrosis in subendocardial regions are seen 2 months after tamoxifen treatment
• hearts are enlarged 2 months after tamoxifen treatment, with impaired contractility and relaxation
• however, thickening of the free wall is not seen
• decrease in left ventricular contractility is seen 21 days after tamoxifen treatment, with a decrease in ejection fraction and mean shortening velocity of circumferential fibers
• contractility and relaxation are moderately altered at 1 month after tamoxifen treatment, however 2 months after tamoxifen treatment, a massive decrease in left ventricle contractility and relaxation are seen, with increased E/Ea ratio, indicating heart failure
• contractility and relaxation are moderately altered at 1 month after tamoxifen treatment, however 2 months after tamoxifen treatment, a massive decrease in left ventricle contractility and relaxation are seen, with increased E/Ea ratio, indicating heart failure
• heart failure is seen 8 to 10 weeks after tamoxifen treatment

muscle
• amount of polymerized F-actin in cardiomyocytes progressively decreases after tamoxifen treatment
• myofibrils at the intercalated disks are often stretched and fragmented following tamoxifen treatment
• Z disks of cardiomyocytes are misaligned and myofibrils are split 60 days after tamoxifen treatment
• 60 days after tamoxifen treatment, cardiac tissue shows a lower density of myofibrils and a defect in demarcation of Z lines and M lines
• 95% of intercalated disks of hearts are enlarged, irregularly shaped, and are thicker 60 days after tamoxifen treatment
• intercalated disks show extensive interdigitation and the presence of lacunae, a widened space at the site of myofibril attachment to the intercalated disks, following tamoxifen treatment
• hearts are enlarged 2 months after tamoxifen treatment, with impaired contractility and relaxation
• however, thickening of the free wall is not seen
• decrease in left ventricular contractility is seen 21 days after tamoxifen treatment, with a decrease in ejection fraction and mean shortening velocity of circumferential fibers
• contractility and relaxation are moderately altered at 1 month after tamoxifen treatment, however 2 months after tamoxifen treatment, a massive decrease in left ventricle contractility and relaxation are seen, with increased E/Ea ratio, indicating heart failure
• contractility and relaxation are moderately altered at 1 month after tamoxifen treatment, however 2 months after tamoxifen treatment, a massive decrease in left ventricle contractility and relaxation are seen, with increased E/Ea ratio, indicating heart failure
• Z disks of cardiomyocytes are misaligned 60 days after tamoxifen treatment




Genotype
MGI:5466537
cn4
Allelic
Composition
Mcattm1.1Ssmi/Mcattm1.1Ssmi
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Mcattm1.1Ssmi mutation (0 available); any Mcat mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• tamoxifen-treated mice appear normal




Genotype
MGI:4441305
cn5
Allelic
Composition
Atp2a2tm1.1Iemr/Atp2a2tm1.1Iemr
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Atp2a2tm1.1Iemr mutation (0 available); any Atp2a2 mutation (46 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• tamoxifen-treated mice do not exhibit myocardial disarray or necrosis
• 4 and 7 weeks after tamoxifen treatment, left atrial diameter is increased compared to in Atp2a2tm1.1Iemr homozygotes
• after tamoxifen treatment
• after tamoxifen treatment
• tamoxifen-treated mice exhibit an increase in the time constant of isovolumetric pressure decay compared with Atp2a2tm1.1Iemr homozygotes
• 7 weeks after tamoxifen treatment, mice exhibit diastolic dysfunction compared with Atp2a2tm1.1Iemr homozygotes
• 4 and 7 weeks after tamoxifen treatment
• 4 weeks after tamoxifen treatment, mice exhibit reduced contractile function compared with Atp2a2tm1.1Iemr homozygotes as determined by Doppler imaging
• at low stimulation frequency, cardiomyocytes from tamoxifen-treated mice exhibit reduced contraction magnitude compared with similarly treated cardiomyocytes from Atp2a2tm1.1Iemr homozygotes
• 7 weeks after tamoxifen treatment, fractional shortening is reduced compared to in Atp2a2tm1.1Iemr homozygotes
• 4 and 7 weeks after tamoxifen treatment, end-diastolic pressure compared to in Atp2a2tm1.1Iemr homozygotes
• 4 and 7 weeks after tamoxifen treatment, mice exhibit reduced maximum positive and minimum derivatives of the left ventricular pressure compared with Atp2a2tm1.1Iemr homozygotes
• 4 and 7 weeks after tamoxifen treatment, anesthetized mice exhibit decreased heart rate compared with Atp2a2tm1.1Iemr homozygotes
• cardiomyocytes from tamoxifen-treated mice exhibit reduced magnitude of calcium ion transients and prolonged time to half decay of calcium ion transients compared with similarly treated cardiomyocytes from Atp2a2tm1.1Iemr homozygotes
• when stimulated at a 6 Hz frequency, cardiomyocytes from tamoxifen-treated mice exhibit shorter diastolic sarcomere length and a greater increase in the contractile response per unit during systole compared with similarly treated cardiomyocytes from Atp2a2tm1.1Iemr homozygotes
• during the slow decline of caffeine transients in the presence of nickel ions, cardiomyocytes from tamoxifen-treated mice exhibit shorter sarcomere length compared with similarly treated cardiomyocytes from Atp2a2tm1.1Iemr homozygotes
• 4 weeks after tamoxifen treatment, cardiomyocytes exhibit reduced sarcoplasmic reticulum calcium ion content compared with cardiomyocytes from Atp2a2tm1.1Iemr homozygotes
• 7 weeks after treatment with tamoxifen, mice exhibit reduced maximal rate of cardiomyocyte relaxation compared with Atp2a2tm1.1Iemr homozygotes
• 7 weeks after tamoxifen treatment

homeostasis/metabolism
• in tamoxifen-treated mice at 4 and 7 weeks

muscle
• 4 weeks after tamoxifen treatment, mice exhibit reduced contractile function compared with Atp2a2tm1.1Iemr homozygotes as determined by Doppler imaging
• at low stimulation frequency, cardiomyocytes from tamoxifen-treated mice exhibit reduced contraction magnitude compared with similarly treated cardiomyocytes from Atp2a2tm1.1Iemr homozygotes
• 7 weeks after tamoxifen treatment, fractional shortening is reduced compared to in Atp2a2tm1.1Iemr homozygotes
• 4 and 7 weeks after tamoxifen treatment, end-diastolic pressure compared to in Atp2a2tm1.1Iemr homozygotes




Genotype
MGI:3832390
cn6
Allelic
Composition
Ldb3tm4Chen/Ldb3tm4Chen
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * Black Swiss * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Ldb3tm4Chen mutation (0 available); any Ldb3 mutation (24 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice die between 1 and 16 weeks after tamoxifen treatment

cardiovascular system
• after tamoxifen treatment
• both ventricles are severely dilated after tamoxifen treatment
• both ventricles are severely dilated after tamoxifen treatment
• decreased heart function one month after tamoxifen treatment
• after tamoxifen treatment

muscle
• after tamoxifen treatment




Genotype
MGI:5576935
cn7
Allelic
Composition
Ryr2tm1Krbr/Ryr2tm1Krbr
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Ryr2tm1Krbr mutation (1 available); any Ryr2 mutation (157 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• tamoxifen-treated mice exhibit sudden cardiac death

cardiovascular system
• in tamoxifen-treated mice
• however, compensatory mechanisms transiently ameliorate detrimental effects
• severe in tamoxifen-treated mice
• in tamoxifen-treated mice
• in tamoxifen-treated mice
• repetitive episodes of tachycardic arrhythmia in tamoxifen-treated mice
• secondary in tamoxifen-treated mice
• distinct T wave in tamoxifen-treated mice
• in tamoxifen-treated mice
• in tamoxifen-treated mice

behavior/neurological
• 4 days after tamoxifen treatment

homeostasis/metabolism
• in tamoxifen-treated mice

muscle
• in tamoxifen-treated mice




Genotype
MGI:5291995
cn8
Allelic
Composition
Cacna1ctm3Hfm/Cacna1ctm4Hfm
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Cacna1ctm3Hfm mutation (1 available); any Cacna1c mutation (60 available)
Cacna1ctm4Hfm mutation (0 available); any Cacna1c mutation (60 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die within 3 weeks of tamoxifen treatment

muscle
• vetricular cardiomyocytes from tamoxifen-treated mice exhibit reduced current-voltage relation of current compared with cells from control mice




Genotype
MGI:5606049
cn9
Allelic
Composition
Ryr2tm1Krbr/Ryr2tm3.1Swch
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Ryr2tm1Krbr mutation (1 available); any Ryr2 mutation (157 available)
Ryr2tm3.1Swch mutation (0 available); any Ryr2 mutation (157 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die starting around 11 days post tamoxifen injection, with most dying by day 14

cardiovascular system
• 12 days post tamoxifen treatment, mice exhibit a reduced basal heart rate
• tamoxifen treated mice, however, do not exhibit stress-induced (by caffeine or epinephrine) ventricular tachyarrhythmias at young or older ages




Genotype
MGI:5446618
cn10
Allelic
Composition
Cacna1ctm1Ggm/Cacna1ctm1Ggm
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Cacna1ctm1Ggm mutation (0 available); any Cacna1c mutation (60 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• average survival time of 11.9 +/- 3 days following tamoxifen treatment for 5 days

cardiovascular system
• increase in ventricular end diastolic volume after tamoxifen treatment
• profound decrease in myocardial contractility, as assessed by fractional shortening, after tamoxifen treatment

muscle
• profound decrease in myocardial contractility, as assessed by fractional shortening, after tamoxifen treatment




Genotype
MGI:4882047
cn11
Allelic
Composition
Ptentm1Hwu/Ptentm1Hwu
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Ptentm1Hwu mutation (3 available); any Pten mutation (40 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• hearts of mutants treated with tamoxifen for 3 weeks to induce cre-expression develop significantly better function recovery in response to 30 min ischemia followed by 120 min reperfusion than controls, showing significantly improved end-diastolic pressure, left ventricle developed pressure (LVDP) and LVDP recoveries, and improved systolic and diastolic contractility of hearts
• at 60 min post reperfusion, recovery of left ventricular diastolic pressure reaches 77.9% of pre-ischemia in hearts versus 44% in controls
• hearts have significantly fewer apoptosis positive cardiomyocytes after ischemia/reperfusion (I/R) injury than controls
• mutants treated with tamoxifen to induce cre-expression exhibit a significant reduction in infarct size after ischemia

homeostasis/metabolism
• hearts of mutants treated with tamoxifen for 3 weeks to induce cre-expression develop significantly better function recovery in response to 30 min ischemia followed by 120 min reperfusion than controls, showing significantly improved end-diastolic pressure, left ventricle developed pressure (LVDP) and LVDP recoveries, and improved systolic and diastolic contractility of hearts
• at 60 min post reperfusion, recovery of left ventricular diastolic pressure reaches 77.9% of pre-ischemia in hearts versus 44% in controls
• hearts have significantly fewer apoptosis positive cardiomyocytes after ischemia/reperfusion (I/R) injury than controls
• mutants treated with tamoxifen to induce cre-expression exhibit a significant reduction in infarct size after ischemia




Genotype
MGI:3818746
cn12
Allelic
Composition
Txniptm1Rlee/Txniptm1Rlee
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Txniptm1Rlee mutation (1 available); any Txnip mutation (34 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• robust increase in glucose uptake in 4-hydroxytamoxifen treated mice compared to controls
• mice treated with 4-hydroxytamoxifen to induce recombination display a decrease in pressure overload induced progressive hypertrophy during the early phase compared to controls

muscle
• robust increase in glucose uptake in 4-hydroxytamoxifen treated mice compared to controls

homeostasis/metabolism
• mice treated with 4-hydroxytamoxifen to induce recombination display a decrease in pressure overload induced progressive hypertrophy during the early phase compared to controls

cellular
• robust increase in glucose uptake in 4-hydroxytamoxifen treated mice compared to controls




Genotype
MGI:5779906
cn13
Allelic
Composition
Mcutm1.1Jmol/Mcutm1.1Jmol
A1cfTg(Myh6-cre/Esr1*)1Jmk/A1cf+
Genetic
Background
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Mcutm1.1Jmol mutation (0 available); any Mcu mutation (16 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• hearts of tamoxifen-treated mice exhibit normal cardiac adaptation to long-term stress induced by transverse aortic constriction
• tamoxifen-treated mice exhibit inhibited acute cardiac mitochondrial calcium uptake compared with control cells
• at 18 weeks, cardiac myocytes from tamoxifen-treated mice challenged with calcium exhibit a severely blunted compared with control cells
• cardiac myocytes from tamoxifen-treated mice exhibit lower sodium-induced calcium efflux rates compared with control cells
• cardiac mitochondria from mice treated with tamoxifen and dobutamine fail to exhibit an increase in calcium unlike control mitochondria
• however, mice exhibit normal baseline mitochondrial calcium levels, response to Ru360, and elevated calcium levels in the mitochondrial following sustained dobutamine treatment
• tamoxifen-treated mice subjected to dobutamine (the beta-adrenergic receptor agonist) exhibit lesser short-term increase in the maximal rate of cardiac pressure compared with control mice
• however, sustained administration of dobutamine at 32 ng/g/min induced similar ventricular pressure
• cardiomyocytes from tamoxifen treated mice fail to exhibit an increase in mitochondrial oxygen consumption and ATP utilization compared with control mice
• however, baseline mitochondrial oxygen consumption and ATP utilization are normal
• in cardiomyocytes from tamoxifen treated mice in response to ionomycin
• in tamoxifen treated mice

homeostasis/metabolism
• under the short warm-up/high-intensity sprinting regimen, tamoxifen-treated mice exhibit reduced running capacity compared with control mice
• however, the difference is lost with a longer warm-up period
• in tamoxifen treated mice

behavior/neurological
• under the short warm-up/high-intensity sprinting regimen, tamoxifen-treated mice exhibit reduced running capacity compared with control mice
• however, the difference is lost with a longer warm-up period

cellular
• in cardiomyocytes from tamoxifen treated mice in response to ionomycin

muscle
• tamoxifen-treated mice exhibit inhibited acute cardiac mitochondrial calcium uptake compared with control cells
• at 18 weeks, cardiac myocytes from tamoxifen-treated mice challenged with calcium exhibit a severely blunted compared with control cells
• cardiac myocytes from tamoxifen-treated mice exhibit lower sodium-induced calcium efflux rates compared with control cells
• cardiac mitochondria from mice treated with tamoxifen and dobutamine fail to exhibit an increase in calcium unlike control mitochondria
• however, mice exhibit normal baseline mitochondrial calcium levels, response to Ru360, and elevated calcium levels in the mitochondrial following sustained dobutamine treatment
• tamoxifen-treated mice subjected to dobutamine (the beta-adrenergic receptor agonist) exhibit lesser short-term increase in the maximal rate of cardiac pressure compared with control mice
• however, sustained administration of dobutamine at 32 ng/g/min induced similar ventricular pressure
• in cardiomyocytes from tamoxifen treated mice in response to ionomycin




Genotype
MGI:4845868
cn14
Allelic
Composition
Pik3cbtm1.1Rzl/Pik3cbtm1.1Rzl
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129S4/SvJaeSor * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Pik3cbtm1.1Rzl mutation (0 available); any Pik3cb mutation (109 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• in tamoxifen-treated mice exhibit normal myocyte reduced inward calcium ion current density
• slightly in tamoxifen-treated mice




Genotype
MGI:4845867
cn15
Allelic
Composition
Pik3catm1.1Rzl/Pik3catm1.1Rzl
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129S4/SvJaeSor * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Pik3catm1.1Rzl mutation (0 available); any Pik3ca mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• in tamoxifen-treated mice
• mildly in tamoxifen-treated mice
• posterior wall thickness in tamoxifen-treated mice is slightly decreased compared to in wild-type mice
• in tamoxifen-treated mice
• myocytes of tamoxifen-treated mice exhibit reduced inward calcium ion current density compared with wild-type cells

muscle
• in tamoxifen-treated mice




Genotype
MGI:3580161
cn16
Allelic
Composition
Cdh2tm1Glr/Cdh2Gt(OST49160)Lex
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129S5/SvEvBrd * 129S6/SvEvTac * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Cdh2Gt(OST49160)Lex mutation (1 available); any Cdh2 mutation (19 available)
Cdh2tm1Glr mutation (1 available); any Cdh2 mutation (19 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants die about 2 months after tamoxifen treatment

cardiovascular system
• modest dilation of the atria after tamoxifen treatment
• after tamoxifen treatment enlarged hyperchromatic myocyte nuclei are seen
• after tamoxifen treatment intercalated disc structures and intercellular space are absent
• after tamoxifen treatment sarcomeres appear distorted and compressed with wider, less dense Z-lines
• after tamoxifen treatment intercalated disc structures are absent
• after tamoxifen treatment hearts appear elongated and flacid
• modest dilation of the ventricles after tamoxifen treatment
• modest dilation of the ventricles after tamoxifen treatment
• left ventricular end-diastolic and end-systolic volume in the cavity are increased and left ventricular ejection fraction is decreased
• about 5 weeks after tamoxifen treatment, mutant heart rate is significantly reduced
• about 6 weeks after tamoxifen treatment, 2 mutants showed abrupt onset of ventricular tachyarrhythmia followed by sudden death
• about 6 weeks after tamoxifen treatment, 2 mutants showed abrupt onset of ventricular tachyarrhythmia followed by sudden death
• tachyarrhythmia is initiated by premature ventricular depolarization

muscle
• after tamoxifen treatment enlarged hyperchromatic myocyte nuclei are seen
• after tamoxifen treatment intercalated disc structures and intercellular space are absent
• after tamoxifen treatment sarcomeres appear distorted and compressed with wider, less dense Z-lines
• after tamoxifen treatment intercalated disc structures are absent
• left ventricular end-diastolic and end-systolic volume in the cavity are increased and left ventricular ejection fraction is decreased




Genotype
MGI:5514169
cn17
Allelic
Composition
Plce1tm2Avsm/Plce1tm2Avsm
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Plce1tm2Avsm mutation (0 available); any Plce1 mutation (50 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• following transverse aortic constriction, mice exhibit diminished cardiac hypertrophy compared with control mice

homeostasis/metabolism
• following transverse aortic constriction, mice exhibit diminished cardiac hypertrophy compared with control mice




Genotype
MGI:5523280
cn18
Allelic
Composition
Tgfbr2tm1.2Hlm/Tgfbr2tm1.2Hlm
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Tgfbr2tm1.2Hlm mutation (0 available); any Tgfbr2 mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• treatment of mice with oral dose of 160 mg/kg BW per day raloxifene for 21 days resulted in similar recombinase activity as the tamoxifen regimen, but does not cause any cardiac dysfunction; lower (20 mg/kg BW) oral tamoxifen treatment for 21 days does not cause dysfunction
• mice die by 6 days post-treatment (80 mg/kg BW IP for 5 days) from severe dilated cardiomyopathy
• oral delivery of 80 mg/kg BW tamoxifen for 7 days does not result in any mortality but treated mice exhibit a significant but reversible dilated cardiomyopathy
• 3 days after oral tamoxifen treatment, cardiac depression peaks with fractional shortening decreasing from 61 to 27% and end-diastolic dimension increasing significantly

mortality/aging
• by 6 days following IP tamoxifen treatment (80 mg/kg BW for 5 days), 60% mortality of treated mice is observed

muscle
• mice die by 6 days post-treatment (80 mg/kg BW IP for 5 days) from severe dilated cardiomyopathy
• oral delivery of 80 mg/kg BW tamoxifen for 7 days does not result in any mortality but treated mice exhibit a significant but reversible dilated cardiomyopathy
• 3 days after oral tamoxifen treatment, cardiac depression peaks with fractional shortening decreasing from 61 to 27% and end-diastolic dimension increasing significantly




Genotype
MGI:4947241
cn19
Allelic
Composition
Juptm1.1Glr/Juptm1.1Glr
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Juptm1.1Glr mutation (1 available); any Jup mutation (139 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• increase in cardiac death compared to controls beginning about 3 months after tamoxifen treatment

cardiovascular system
N
• unlike in human patients with Arrhythmogenic Right Ventricular Dysplasia replacement of myocytes with adipocytes is not seen in tamoxifen treated mice and tamoxifen treated mice are not more susceptible to induced arrhythmias
• decrease in the number and length of desmosomes in tamoxifen treated mice
• adherens-type junctions with less submembranous electron-dense material are prominently seen in tamoxifen treated mice
• mislocalization of desmosomal proteins to the intercalated disc in tamoxifen treated mice
• increase in cardiomyocyte cross sectional area with age in tamoxifen treated mice
• increase in the heart to body weight ratio with age in tamoxifen treated mice
• by about 5 months after tamoxifen treatment
• mild left ventricle hypertrophy in tamoxifen treated mice
• modest left ventricle dilation in tamoxifen treated mice
• progressive thinning of the right ventricular free wall is seen after tamoxifen treatment
• by about 5 months after tamoxifen treatment
• focal areas of myocyte loss and replacement with fibrous tissue are seen after tamoxifen treatment
• increased apoptosis is seen at 5 months after tamoxifen treatment
• apoptotic cells are associated with fibrotic areas
• heart failure is seen in some tamoxifen treated mice
• reduction of left ventricular fractional shortening and ejection fraction in tamoxifen treated mice
• infiltration of activated macrophages/monocytes in areas adjacent to apoptotic myocytes in tamoxifen treated mice
• neutrophil infiltrations are also seen in tamoxifen treated mice

muscle
• decrease in the number and length of desmosomes in tamoxifen treated mice
• adherens-type junctions with less submembranous electron-dense material are prominently seen in tamoxifen treated mice
• mislocalization of desmosomal proteins to the intercalated disc in tamoxifen treated mice
• increase in cardiomyocyte cross sectional area with age in tamoxifen treated mice
• reduction of left ventricular fractional shortening and ejection fraction in tamoxifen treated mice
• cardiomyocyte sarcomeres have wider, less dense Z lines in tamoxifen treated mice
• cardiomyocyte sarcomeres appear distorted and compressed in tamoxifen treated mice
• decreased cardiomyocyte sarcomere length in tamoxifen treated mice

homeostasis/metabolism
• seen at 9 - 12 months after tamoxifen treatment, associated with heart failure
• increase in the IL6 and IL1B levels in heart lysates from tamoxifen treated mice
• increase in cytokine expression is associated with the severity of myocyte loss

immune system
• infiltration of activated macrophages/monocytes in areas adjacent to apoptotic myocytes in tamoxifen treated mice
• neutrophil infiltrations are also seen in tamoxifen treated mice
• increase in the IL6 and IL1B levels in heart lysates from tamoxifen treated mice
• increase in cytokine expression is associated with the severity of myocyte loss

respiratory system
• seen at 9 - 12 months after tamoxifen treatment, associated with heart failure




Genotype
MGI:5688487
cn20
Allelic
Composition
Wdr1tm1.1Zzy/Wdr1tm1.1Zzy
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Wdr1tm1.1Zzy mutation (0 available); any Wdr1 mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• when treated with tamoxifen at 2 months of age, mice begin to die at 56 days after the first tamoxifen injection, and none survive past 104 days

cardiovascular system
• F-actin accumulations are observed within myofibrils at 1 month after the first tamoxifen injection
• cardiomyocyte size is increased at 1 month after the first tamoxifen injection
• in male mice, the heart weight/body weight ratio begins to increase at 1 month after the first tamoxifen injection
• however, no significant changes are observed in tamoxifen-treated female mice
• tamoxifen-treated mice exhibit a milder heart hypertrophy relative to that observed in mice that are homozygous for Wdr1tm1.1Zzy and hemizygous for Tg(Myhc-cre)1Xya

muscle
• F-actin accumulations are observed within myofibrils at 1 month after the first tamoxifen injection
• cardiomyocyte size is increased at 1 month after the first tamoxifen injection




Genotype
MGI:3580162
cn21
Allelic
Composition
Cdh2tm1Glr/Cdh2tm1Hyn
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Cdh2tm1Glr mutation (1 available); any Cdh2 mutation (19 available)
Cdh2tm1Hyn mutation (1 available); any Cdh2 mutation (19 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants die about 2 months after tamoxifen treatment

cardiovascular system
• modest dilation of the atria after tamoxifen treatment
• after tamoxifen treatment enlarged hyperchromatic myocyte nuclei are seen
• after tamoxifen treatment intercalated disc structures and intercellular space are absent
• after tamoxifen treatment sarcomeres appear distorted and compressed with wider, less dense Z-lines
• after tamoxifen treatment intercalated disc structures are absent
• after tamoxifen treatment hearts appear elongated and flacid
• modest dilation of the ventricles after tamoxifen treatment
• modest dilation of the ventricles after tamoxifen treatment
• eft ventricular end-diastolic and end-systolic volume in the cavity are increased and left ventricular ejection fraction is decreased
• about 5 weeks after tamoxifen treatment, mutant heart rate is significantly reduced
• about 6 weeks after tamoxifen treatment, 2 mutants showed abrupt onset of ventricular tachyarrhythmia followed by sudden death
• about 6 weeks after tamoxifen treatment, 2 mutants showed abrupt onset of ventricular tachyarrhythmia followed by sudden death
• tachyarrhythmia is initiated by premature ventricular depolarization

muscle
• after tamoxifen treatment enlarged hyperchromatic myocyte nuclei are seen
• after tamoxifen treatment intercalated disc structures and intercellular space are absent
• after tamoxifen treatment sarcomeres appear distorted and compressed with wider, less dense Z-lines
• after tamoxifen treatment intercalated disc structures are absent
• eft ventricular end-diastolic and end-systolic volume in the cavity are increased and left ventricular ejection fraction is decreased




Genotype
MGI:5523277
cn22
Allelic
Composition
Tgfbr1tm1.1Karl/Tgfbr1tm1.1Karl
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129S/Sv * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Tgfbr1tm1.1Karl mutation (1 available); any Tgfbr1 mutation (16 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• by 6 days following IP tamoxifen treatment (80 mg/kg BW for 5 days), 60% mortality of treated mice is observed

cardiovascular system
N
• treatment of mice with oral dose of 160 mg/kg BW per day raloxifene for 21 days resulted in similar recombinase activity as the tamoxifen regimen, but does not cause any cardiac dysfunction; lower (20 mg/kg BW) oral tamoxifen treatment for 21 days does not cause dysfunction
• mice die by 6 days post-treatment (80 mg/kg BW IP for 5 days) from severe dilated cardiomyopathy
• oral delivery of 80 mg/kg BW tamoxifen for 7 days does not result in any mortality but treated mice exhibit a significant but reversible dilated cardiomyopathy
• 3 days after oral tamoxifen treatment, cardiac depression peaks with fractional shortening decreasing from 61 to 27% and end-diastolic dimension increasing significantly

muscle
• mice die by 6 days post-treatment (80 mg/kg BW IP for 5 days) from severe dilated cardiomyopathy
• oral delivery of 80 mg/kg BW tamoxifen for 7 days does not result in any mortality but treated mice exhibit a significant but reversible dilated cardiomyopathy
• 3 days after oral tamoxifen treatment, cardiac depression peaks with fractional shortening decreasing from 61 to 27% and end-diastolic dimension increasing significantly




Genotype
MGI:4888970
cn23
Allelic
Composition
Hcn4tm1.1Ggc/Hcn4tm1.1Ggc
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129S/SvEv * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Hcn4tm1.1Ggc mutation (0 available); any Hcn4 mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• develop severe bradycardia when injected daily with tamoxifen which leads eventually to death
• heart rate reduced by 32% after 2 days of treatment and by 47% after 6 days
• isolated cells from the sino-atrial node of mice treated with tamoxifen beat spontaneously but more slowly than control cells and become progressively slower as treatment is continued to 5 days
• mice injected with isoproterenol experience heart beat acceleration similar to that occurring in control mice
• when injected daily with tamoxifen, atrioventricular block becomes a 2nd degree block
• conduction ratio progresses from 2:1 to 4:1 or more
• when mice are injected daily with tamoxifen, a prolonged PQ interval is observed
• f-channel current densities from atrioventricular cells isolated from mice after 2 and 5 days of treatment with tamoxifen are lower than for control cells
• there is a time dependent decrease in f-channel conductance

mortality/aging
• no mice survive beyond 8.5 days of treatment with tamoxifen




Genotype
MGI:3713115
cn24
Allelic
Composition
Atg5tm1Myok/Atg5tm1Myok
A1cfTg(Myh6-cre/Esr1*)1Jmk/?
Genetic
Background
involves: 129S/SvEv * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Atg5tm1Myok mutation (2 available); any Atg5 mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• cardiomyocyte fiber cross-sectional area is increased following tamoxifen treatment
• however, cardiomyocyte fibers are otherwise normal
• increase in the heart to body weight ratio following tamoxifen treatment
• following tamoxifen treatment
• following tamoxifen treatment
• calcium cycling is impaired following tamoxifen treatment
• decrease in the autophagy levels following tamoxifen treatment

respiratory system
• increase in the lung to body weight ratio following tamoxifen treatment

muscle
• cardiomyocyte fiber cross-sectional area is increased following tamoxifen treatment
• however, cardiomyocyte fibers are otherwise normal
• following tamoxifen treatment




Genotype
MGI:3844714
cn25
Allelic
Composition
Ptgs2tm1Gaf/Ptgs2tm1Gaf
A1cfTg(Myh6-cre/Esr1*)1Jmk/?
Genetic
Background
involves: 129/Sv * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Ptgs2tm1Gaf mutation (0 available); any Ptgs2 mutation (32 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• hypertrophy of cardiomyocytes occurs after 6 weeks of aortic banding to mice that have had cre expression induced
• left ventricular end systolic volume is increased after cre induction from 0.017 cm3/g to 0.021 cm3/g
• after cre induction, the left ventricular ejection fraction is depressed from 0.65 cm3/g to 0.60 cm3/g
• heart rate is depressed after cre induction from 443 bpm to 441 bpm
• male mice with cre induction and intracardiac electrical stimulation have more ventricular tachycardia episodes than controls (17 vs. 3)
• duration of these episodes are also about 3-fold longer than controls

growth/size/body
• mice in which cre expression is induced have more weight loss than controls in response to exercise

homeostasis/metabolism
• mice with cre expression have a reduced exercise capacity

muscle
• hypertrophy of cardiomyocytes occurs after 6 weeks of aortic banding to mice that have had cre expression induced
• after cre induction, the left ventricular ejection fraction is depressed from 0.65 cm3/g to 0.60 cm3/g

behavior/neurological
• mice with cre expression have a reduced exercise capacity




Genotype
MGI:5504499
cn26
Allelic
Composition
Ctnna1tm1Efu/Ctnna1tm1Efu
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Ctnna1tm1Efu mutation (1 available); any Ctnna1 mutation (120 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• progressive 8 months after tamoxifen treatment

muscle
• progressive 8 months after tamoxifen treatment




Genotype
MGI:5569640
cn27
Allelic
Composition
Dmdtm1.1Know/Dmdtm1.1Know
Tg(Myh6-2A)#Know/0
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: BALB/c * C3H * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Dmdtm1.1Know mutation (0 available); any Dmd mutation (159 available)
Tg(Myh6-2A)#Know mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Inhibition of dilated cardiomyopathy in Dmdtm1.1Know/Dmdtm1.1Know Tg(Myh6-2A)#Know/0 A1cfTg(Myh6-cre/Esr1*)1Jmk/0 mice

cardiovascular system
• less severe fibrosis in tamoxifen-treated mice
• improved cardiac function in tamoxifen-treated mice
• improved cardiac function in tamoxifen-treated mice
• less severe cardiomyopathy in tamoxifen-treated mice

homeostasis/metabolism
• tamoxifen-treated mice exhibit less severe cardiomyopathy, cardiac fibrosis and improved cardiac function compared with control mice

muscle
• improved cardiac function in tamoxifen-treated mice
• less severe cardiomyopathy in tamoxifen-treated mice




Genotype
MGI:5614265
cn28
Allelic
Composition
Tnni3ktm1Tfo/Tnni3ktm1Tfo
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Tnni3ktm1Tfo mutation (0 available); any Tnni3k mutation (22 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• tamoxifen-treated mice exhibit normal left ventricle function and cardiac morphometry and normal left ventricular remodeling after permanent occlusion myoinfarction
• decreased cell death in tamoxifen-treated mice following ischemic injury
• following ischemic/reperfusion injury, tamoxifen-treated mice exhibit decreased infarct size and cardiomyocyte cell death compared with wild-type mice
• however, normal left ventricular remodeling after permanent occlusion myoinfarction
• in tamoxifen-treated mice following ischemic/reperfusion injury

homeostasis/metabolism
• following ischemic/reperfusion injury, tamoxifen-treated mice exhibit decreased infarct size and cardiomyocyte cell death compared with wild-type mice
• however, normal left ventricular remodeling after permanent occlusion myoinfarction
• in tamoxifen-treated mice following ischemic/reperfusion injury




Genotype
MGI:5588664
cn29
Allelic
Composition
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Tspotm1.1Maf/Tspotm1.1Maf
Genetic
Background
involves: C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Tspotm1.1Maf mutation (1 available); any Tspo mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• tamoxifen treated mice show a similiar response to ischemia/reperfusion injury as controls




Genotype
MGI:5603568
cn30
Allelic
Composition
Akap6tm1.1Mskf/Akap6tm1.1Mskf
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Akap6tm1.1Mskf mutation (1 available); any Akap6 mutation (54 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• following cardiac stress by long term transverse aortic constriction (LT-TAC), mice administered tamoxifen exhibit increased left atrial weight (35%) as compared controls undergoing a sham procedure, but less than the increase (50%) in controls subjected to the same regime
• following 2 weeks of TAC or isoproterenol infusion, left venticle (LV) myocytes from mice administered tamoxifen exhibit an increase in cross section area, but to a much lessor extent than controls subjected to the same regime
• following a LT-TAC, mice administered tamoxifen die as a result of congenital heart failure, but exhibit greater survival than controls subjected to the same regime (6% vs 29%) and do not exhibit pulmonary edema
• following a long term (LT) TAC, mice administered tamoxifen die as a result of congenital heart failure, but exhibit greater survival than controls subjected to the same regime (6% vs 29%) and do not exhibit pulmonary edema
• following 2 weeks of TAC or isoproterenol infusion, mice administered tamoxifen exhibit increased left ventricular (LV) wall thickness, but to a much lessor extent than controls subjected to the same regime
• following 2 weeks of cardiac stress by transverse aortic constriction (TAC) or isoproterenol infusion, mice administered tamoxifen exhibit increased biventricular weight, but to a much lessor extent than controls subjected to the same regime
• following a 5 week swimming regime, mice administered tamoxifen exhibit an increase in biventricular weight gain, but to a lessor extent than controls subjected to the same regime (13% vs 5%)
• following a long term LT-TAC, mice administered tamoxifen exhibit increased collagen deposistion, but 78% less collagen deposition as compared controls subjected to the same regime
• following a 5 week swimming regime, mice administered tamoxifen exhibit lower heart rate than controls subjected to the same regime
• following a long term LT-TAC, mice administered tamoxifen exhibit increased apoptosis, but 75% less myocardial apoptosis as compared controls subjected to the same regime

cellular
• following a long term LT-TAC, mice administered tamoxifen exhibit increased apoptosis, but 75% less myocardial apoptosis as compared controls subjected to the same regime

muscle
• following 2 weeks of TAC or isoproterenol infusion, left venticle (LV) myocytes from mice administered tamoxifen exhibit an increase in cross section area, but to a much lessor extent than controls subjected to the same regime
• following a long term LT-TAC, mice administered tamoxifen exhibit increased apoptosis, but 75% less myocardial apoptosis as compared controls subjected to the same regime




Genotype
MGI:5426794
cn31
Allelic
Composition
Tg(CAG-DMPK*)1323Coop/0
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Tg(CAG-DMPK*)1323Coop mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants treated with tamoxifen at 8-9 weeks of age to induce Cre-mediated recombination die within 2 weeks of tamoxifen injection

cardiovascular system
• cardiomyocyte cytoplasm of tamoxifen treated mutants appears pale in patchy areas and contains variably prominent numbers of pink granules; focally abundant mitochondria correlate with the pink granules
• in some myocytes of tamoxifen treated mutants, aggregates of proliferating membranes of the sarcoplasmic reticulum are seen
• however, sarcomeres and Z-lines appear normal
• mutants treated with tamoxifen exhibit myocyte hypertrophy with enlarged, irregular myocyte nuclei
• dilation of the left ventricle after treatment with tamoxifen
• thinning of the left ventricular wall after treatment with tamoxifen
• rare degenerating myocytes and focal areas of mild interstitial fibrosis are seen in mutants treated with tamoxifen
• mutants treated with tamoxifen exhibit cardiac dysfunction in both systolic and diastolic parameters
• mutants treated with tamoxifen at 8-9 weeks of age to induce Cre-mediated recombination develop dilated cardiomyopathy
• peak early diastolic filling velocity is decreased by more than 30% in mutants treated with tamoxifen
• systolic function of mutants treated with tamoxifen exhibits a 50% or greater decrease in peak aortic flow velocity and both mean and peak acceleration
• isovolumic relaxation time is prolonged by more than 50% in mutants treated with tamoxifen
• standard deviation of RR intervals is increased 5-fold after tamoxifen administration
• at 4 days after the last day of tamoxifen administration, mice show 2:1 atrioventricular block
• progressive lengthening of the PR interval is seen beginning 2 days after the last day of tamoxifen administration
• widening of the QRS complex is seen beginning 2 days after the last day of tamoxifen administration

muscle
• cardiomyocyte cytoplasm of tamoxifen treated mutants appears pale in patchy areas and contains variably prominent numbers of pink granules; focally abundant mitochondria correlate with the pink granules
• in some myocytes of tamoxifen treated mutants, aggregates of proliferating membranes of the sarcoplasmic reticulum are seen
• however, sarcomeres and Z-lines appear normal
• mutants treated with tamoxifen exhibit myocyte hypertrophy with enlarged, irregular myocyte nuclei
• mutants treated with tamoxifen at 8-9 weeks of age to induce Cre-mediated recombination develop dilated cardiomyopathy
• systolic function of mutants treated with tamoxifen exhibits a 50% or greater decrease in peak aortic flow velocity and both mean and peak acceleration
• isovolumic relaxation time is prolonged by more than 50% in mutants treated with tamoxifen

Mouse Models of Human Disease
OMIM ID Ref(s)
Myotonic Dystrophy 1; DM1 160900 J:127391




Genotype
MGI:5444495
cn32
Allelic
Composition
Irx3tm3Hui/Irx3tm3Hui
Irx5tm3Hui/Irx5tm3Hui
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Irx3tm3Hui mutation (0 available); any Irx3 mutation (9 available)
Irx5tm3Hui mutation (0 available); any Irx5 mutation (11 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• in tamoxifen treated mice
• in tamoxifen treated mice




Genotype
MGI:5315861
cn33
Allelic
Composition
Abcb8tm1Hard/Abcb8tm1Hard
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Abcb8tm1Hard mutation (0 available); any Abcb8 mutation (11 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• subcellular disorganization, with accumulation of vacuoles, mitochondria showing diversity in size, profoundly disrupted alignment, and a rounder and more densely packed appearance after tamoxifen treatment
• loss of mitochondrial cristae and smaller average mitochondria size after tamoxifen treatment
• elevated mitochondrial iron content but not heme levels 4 weeks after tamoxifen treatment
• distorted and wavy myofiber architecture 4 weeks after tamoxifen treatment
• mitochondrial deformities accompanied by electron-dense material are present after tamoxifen treatment
• 8 weeks after tamoxifen treatment
• increased left ventricular diastolic diameter at 8 weeks after tamoxifen treatment
• 8 weeks after tamoxifen treatment
• elevated lipid peroxidation and reactive oxygen species after tamoxifen treatment
• as early as 4 weeks after tamoxifen treatment
• reduced heart pump function as measured by fractional shortening and ejection fraction 4 and 8 weeks after tamoxifen treatment
• decreased strength of contraction (dP/dtmax) at 8 weeks after tamoxifen treatment
• decreased relaxation (dP/dtmin) at 8 weeks after tamoxifen treatment
• lower end systolic pressure at 8 weeks after tamoxifen treatment
• mild after tamoxifen treatment

homeostasis/metabolism
• elevated mitochondrial iron content but not heme levels 4 weeks after tamoxifen treatment

muscle
• distorted and wavy myofiber architecture 4 weeks after tamoxifen treatment
• mitochondrial deformities accompanied by electron-dense material are present after tamoxifen treatment
• reduced heart pump function as measured by fractional shortening and ejection fraction 4 and 8 weeks after tamoxifen treatment
• decreased strength of contraction (dP/dtmax) at 8 weeks after tamoxifen treatment
• decreased relaxation (dP/dtmin) at 8 weeks after tamoxifen treatment
• mild after tamoxifen treatment




Genotype
MGI:3812384
cn34
Allelic
Composition
Cxadrtm1Mgot/Cxadrtm1Mgot
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Cxadrtm1Mgot mutation (0 available); any Cxadr mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• the volume of the atrioventricular node is reduced by about a third compared to controls 8 weeks after cre induction
• sinus node tachycardia is noted in about 17% of mice that have had cre expression induced
• sinus bradycardia is observed in about a third of the mice that have had cre expression induced
• long term monitoring of mice indicates a general increase in heart rate in the weeks after induction of cre
• the prolongation of the PR interval is a hallmark of atrioventricular block
• partial failure of AV conduction (25%) or total dissociation of atrial and ventricular rhythms (37.5%) occurs by 4 weeks after cre induction
• half of the mice have accelerated junctional rhythms that originate in the AV node
• not all the excitations successfully traverse the AV node at slower heart rates (i.e. increased Wenckebach periodity)
• dye-coupling experiments reveals leakiness between cardiomyocytes starting three weeks after cre induction
• mice have a prolonged PR-interval after induction of cre expression
• the length of the interval increases the longer after induction of cre
• by 4 weeks after induction of cre, the length of the interval has more than doubled




Genotype
MGI:5750664
cn35
Allelic
Composition
Senp2tm1.1Eyeh/Senp2tm1.1Eyeh
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Senp2tm1.1Eyeh mutation (0 available); any Senp2 mutation (29 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• tamoxifen treated mice do not die prematurely

nervous system
N
• tamoxifen treated mice do not develop seizures




Genotype
MGI:3815316
cn36
Allelic
Composition
Hif1atm1Stom/Hif1atm1Stom
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
Hif1atm1Stom mutation (0 available); any Hif1a mutation (22 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• reduced number of microvessels form 2 weeks after transverse aortic constriction
• attenuated development of hypertrophy as a result of transverse aortic restriction
• impaired cardiac function




Genotype
MGI:5523279
ot37
Allelic
Composition
A1cfTg(Myh6-cre/Esr1*)1Jmk/0
Genetic
Background
involves: 129S/Sv * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (2 available); any A1cf mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• patchy interstitial mononuclear infiltration is observed at day 10, but resolves by 3 weeks; no myocyte hypertrophy is observed
• mice die by 6 days post-treatment (80 mg/kg BW IP for 5 days) from severe dilated cardiomyopathy
• oral delivery of 80 mg/kg BW tamoxifen for 7 days does not result in any mortality but treated mice exhibit a significant but reversible dilated cardiomyopathy
• 3 days after oral tamoxifen treatment, cardiac depression peaks with fractional shortening decreasing from 61 to 27% and end-diastolic dimension increasing
• marked transient systolic and diastolic depression occurs, with full recovery observed by 3 weeks after stopping tamoxifen treatment

muscle
• mice die by 6 days post-treatment (80 mg/kg BW IP for 5 days) from severe dilated cardiomyopathy
• oral delivery of 80 mg/kg BW tamoxifen for 7 days does not result in any mortality but treated mice exhibit a significant but reversible dilated cardiomyopathy
• 3 days after oral tamoxifen treatment, cardiac depression peaks with fractional shortening decreasing from 61 to 27% and end-diastolic dimension increasing
• marked transient systolic and diastolic depression occurs, with full recovery observed by 3 weeks after stopping tamoxifen treatment





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last database update
07/19/2016
MGI 6.04
The Jackson Laboratory