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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Myh11-icre/ERT2)1Soff
transgene insertion 1, Stefan Offermanns
MGI:3819270
Summary 18 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Cyb5r3tm1c(KOMP)Wtsi/Cyb5r3tm1c(KOMP)Wtsi
Tg(Myh11-icre/ERT2)1Soff/0
B6.Cg-Cyb5r3tm1c(KOMP)Wtsi Tg(Myh11-icre/ERT2)1Soff MGI:6379024
cn2
Gucy1b1tm1.2Frb/Gucy1b1tm1.2Frb
X/Tg(Myh11-icre/ERT2)1Soff
B6.Cg-Gucy1b1tm1.2Frb Tg(Myh11-icre/ERT2)1Soff MGI:5432120
cn3
Atf4tm1.1Cmad/Atf4tm1.1Cmad
Tg(Myh11-icre/ERT2)1Soff/?
D2.Cg-Atf4tm1.1Cmad Tg(Myh11-icre/ERT2)1Soff MGI:5812899
cn4
Gt(ROSA)26Sortm2(ATF4)Myz/Gt(ROSA)26Sortm2(ATF4)Myz
Tg(Myh11-icre/ERT2)1Soff/?
either: D2.Cg-Atf4tm1.1Cmad Tg(Myh11-icre/ERT2)1Soff or B6.Cg-Atf4tm1.1Cmad Tg(Myh11-icre/ERT2)1Soff MGI:5812901
cn5
Acvrl1tm2.1Spo/Acvrl1tm2.1Spo
Tg(Myh11-icre/ERT2)1Soff/0
involves: 129 * FVB/N MGI:5775200
cn6
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaqtm2Soff
X/Tg(Myh11-icre/ERT2)1Soff
involves: 129P2/OlaHsd * 129S7/SvEvBrd * FVB/N MGI:3819271
cn7
Engtm2.1Hma/Engtm2.1Hma
Tg(Myh11-icre/ERT2)1Soff/0
involves: 129P2/OlaHsd * FVB/N MGI:5775198
cn8
Ano1tm1.1Cahb/Ano1tm1.1Cahb
Tg(Myh11-icre/ERT2)1Soff/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N MGI:5588166
cn9
Gna12tm1Citb/Gna12tm1Citb
Gna13tm2.1Soff/Gna13tm2.1Soff
X/Tg(Myh11-icre/ERT2)1Soff
involves: 129S1/Sv * FVB/N MGI:3819345
cn10
Kcnma1tm1Ruth/Kcnma1tm2.1Ruth
X/Tg(Myh11-icre/ERT2)1Soff
involves: 129/Sv * C57BL/6 * FVB/N MGI:3845037
cn11
Rgs2tm1.1Kjb/Rgs2tm1.1Kjb
X/Tg(Myh11-icre/ERT2)1Soff
involves: 129X1/SvJ * C57BL/6 * FVB/N MGI:5426419
cn12
Tg(ACTB-EGFP,-Kcnj8*G343D)9Nich/0
Tg(Myh11-icre/ERT2)1Soff/0
involves: C57BL/6 * CBA * FVB/N MGI:6236323
cn13
Tg(ACTB-EGFP,-Kcnj8)1Nich/0
Tg(Myh11-icre/ERT2)1Soff/0
involves: C57BL/6 * CBA * FVB/N MGI:6236322
cn14
Tg(ACTB-EGFP,-Kcnj8*Q53R*G343D)1Nich/0
Tg(Myh11-icre/ERT2)1Soff/0
involves: C57BL/6 * CBA * FVB/N MGI:6236324
cn15
Arhgef1tm1Rmt/Arhgef1tm1Rmt
X/Tg(Myh11-icre/ERT2)1Soff
involves: C57BL/6 * FVB/N MGI:4442363
cn16
Ppp1r12aem1Sfsh/Ppp1r12a+
Tg(Myh11-icre/ERT2)1Soff/0
involves: C57BL/6J * FVB/N MGI:5776052
cn17
Rgs4tm1Sdlk/Rgs4tm1Sdlk
Tg(Myh11-icre/ERT2)1Soff/?
involves: FVB/N MGI:5605986
cn18
Tg(ACTB-EGFP,-Kcnj8*)1Wco/0
Tg(Myh11-icre/ERT2)1Soff/0
involves: FVB/N MGI:6275077


Genotype
MGI:6379024
cn1
Allelic
Composition
Cyb5r3tm1c(KOMP)Wtsi/Cyb5r3tm1c(KOMP)Wtsi
Tg(Myh11-icre/ERT2)1Soff/0
Genetic
Background
B6.Cg-Cyb5r3tm1c(KOMP)Wtsi Tg(Myh11-icre/ERT2)1Soff
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cyb5r3tm1c(KOMP)Wtsi mutation (0 available); any Cyb5r3 mutation (17 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• heart rates are lower over a total 24 hour period in tamoxifen-induced mice
• tamoxifen-induced mice infused with angiotensin II show decreased heart rate compared to controls during the first 7 days of angiotensin treatment but while heart rate in wild-type mice declines between 8-9 days of angiotensin II, mutant mice maintain a consistent heart rate
• mice are more susceptible to hypertensive agonists and have impaired ability to mitigate the effects of angiotensin II
• tamoxifen-induced mice exhibit a 5.84-mmHg increase in mean arterial pressure over a 24 hour period, with higher systolic and diastolic pressures
• tamoxifen-induced mice infused with angiotensin II to drive soluble guanylyl cyclase oxidation and elevate blood pressure exhibit a 14.75-mmHg blood pressure increase, with an increase in both mean arterial systolic and diastolic pressures
• hypertensive (via angiotensin II treatment) tamoxifen-induced mice show increased vasoconstriciton of mesenteric arteries in response to the thromboxane mimetic U46619
• however, vasoconstriction of non-angiotensin treated mesenteric arteries with U46619 shows no difference between wild-type and tamoxifen-treated mutant mice
• tamoxifen-induced mice exhibit impaired acetylcholine-induced vasodilation in mesenteric arteries
• tamoxifen-induced mice exhibit a slight, but significant, impairment in vasodilation response of mesenteric arteries to BAY 58-2667, a soluble guanylyl cyclase heme-independent activator
• however, mice do not show differences in sodium nitroprusside, a nitric oxide donor molecule, induced vasodilation in mesenteric arteries
• tamoxifen-induced mice treated with angiotensin II to induce hypertension show impaired acetylcholine-mediated vasodilation
• hypertensive (via angiotensin II treatment) tamoxifen-induced mice exhibit diminished nitric oxide-dependent vasodilation in mesenteric arteries
• aortas from hypertensive tamoxifen-induced mice are less responsive to acetylcholine-mediated vasodilation
• however, aortas show no difference in phenylephrine-mediated vasoconstriction or vasodilation via SNP or BAY 58-2667
• hypertensive tamoxifen-induced mice exhibit increased vasodilation responsiveness to soluble guanylyl cyclase heme-independent activator BAY 58-2667

homeostasis/metabolism
• acute injection of BAY 58-2667 in angiotensin II-treated hypertensive tamoxifen-induced mice results in a greater blood pressure reduction than in controls

hematopoietic system
• tamoxifen-induced mice exhibit fewer circulating monocytes compared to wild-type mice
• however, white blood cell, red blood cell, platelet, lymphocyte, and granulocyte counts are normal and hematocrit and hemoglobin levels are normal

immune system
• tamoxifen-induced mice exhibit fewer circulating monocytes compared to wild-type mice
• however, white blood cell, red blood cell, platelet, lymphocyte, and granulocyte counts are normal and hematocrit and hemoglobin levels are normal

muscle
• hypertensive (via angiotensin II treatment) tamoxifen-induced mice show increased vasoconstriciton of mesenteric arteries in response to the thromboxane mimetic U46619
• however, vasoconstriction of non-angiotensin treated mesenteric arteries with U46619 shows no difference between wild-type and tamoxifen-treated mutant mice
• tamoxifen-induced mice exhibit impaired acetylcholine-induced vasodilation in mesenteric arteries
• tamoxifen-induced mice exhibit a slight, but significant, impairment in vasodilation response of mesenteric arteries to BAY 58-2667, a soluble guanylyl cyclase heme-independent activator
• however, mice do not show differences in sodium nitroprusside, a nitric oxide donor molecule, induced vasodilation in mesenteric arteries
• tamoxifen-induced mice treated with angiotensin II to induce hypertension show impaired acetylcholine-mediated vasodilation
• hypertensive (via angiotensin II treatment) tamoxifen-induced mice exhibit diminished nitric oxide-dependent vasodilation in mesenteric arteries
• aortas from hypertensive tamoxifen-induced mice are less responsive to acetylcholine-mediated vasodilation
• however, aortas show no difference in phenylephrine-mediated vasoconstriction or vasodilation via SNP or BAY 58-2667
• hypertensive tamoxifen-induced mice exhibit increased vasodilation responsiveness to soluble guanylyl cyclase heme-independent activator BAY 58-2667




Genotype
MGI:5432120
cn2
Allelic
Composition
Gucy1b1tm1.2Frb/Gucy1b1tm1.2Frb
X/Tg(Myh11-icre/ERT2)1Soff
Genetic
Background
B6.Cg-Gucy1b1tm1.2Frb Tg(Myh11-icre/ERT2)1Soff
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gucy1b1tm1.2Frb mutation (0 available); any Gucy1b1 mutation (29 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• after more than 50 days of tamoxifen treatment, mice treated with L-NAME fail to exhibit an increase in systolic blood pressure compared with wild-type mice
• in tamoxifen-treated mice
• after more than 50 days of tamoxifen treatment, mice lose aortic relaxation induced by NO, carbachol or sildenafil unlike control mice
• however, mice exhibit normal relaxation in response to 8-Br-cGMP or atrial natriuretic peptide

muscle
• after more than 50 days of tamoxifen treatment, mice lose aortic relaxation induced by NO, carbachol or sildenafil unlike control mice
• however, mice exhibit normal relaxation in response to 8-Br-cGMP or atrial natriuretic peptide




Genotype
MGI:5812899
cn3
Allelic
Composition
Atf4tm1.1Cmad/Atf4tm1.1Cmad
Tg(Myh11-icre/ERT2)1Soff/?
Genetic
Background
D2.Cg-Atf4tm1.1Cmad Tg(Myh11-icre/ERT2)1Soff
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atf4tm1.1Cmad mutation (1 available); any Atf4 mutation (19 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• following nephrectomy (to induce chronic kidney disease) and administration of tamoxifen, mice developed smaller calcified medial lesions than nephrectomized controls and similar to sham-operated controls

homeostasis/metabolism
N
• following nephrectomy (to induce chronic kidney disease) and administration of tamoxifen, levels of serum creatinine, phosphorus, calcium, cholesterol and triglyceride are similar to levels in nephrectomized wild-type mice
• following nephrectomy (to induce chronic kidney disease) and administration of tamoxifen, aortic calcium content was lower than nephrectomized controls, but higher than sham-operated controls




Genotype
MGI:5812901
cn4
Allelic
Composition
Gt(ROSA)26Sortm2(ATF4)Myz/Gt(ROSA)26Sortm2(ATF4)Myz
Tg(Myh11-icre/ERT2)1Soff/?
Genetic
Background
either: D2.Cg-Atf4tm1.1Cmad Tg(Myh11-icre/ERT2)1Soff or B6.Cg-Atf4tm1.1Cmad Tg(Myh11-icre/ERT2)1Soff
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm2(ATF4)Myz mutation (1 available); any Gt(ROSA)26Sor mutation (795 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• following administration of tamoxifen, mice develop severe medial calcification in aortic sinuses
• following administration of tamoxifen, there is an increase of apoptotic cells in the aorta

cellular
• following administration of tamoxifen, there is an increase of apoptotic cells in the aorta

homeostasis/metabolism
N
• following administration of tamoxifen, levels of phosphorus, calcium, cholesterol and triglyceride are similar to controls

muscle
• following administration of tamoxifen, there is an increase of apoptotic cells in the aorta




Genotype
MGI:5775200
cn5
Allelic
Composition
Acvrl1tm2.1Spo/Acvrl1tm2.1Spo
Tg(Myh11-icre/ERT2)1Soff/0
Genetic
Background
involves: 129 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Acvrl1tm2.1Spo mutation (0 available); any Acvrl1 mutation (15 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• tamoxifen-treated mice do not develop arteriovenous (AV) shunts in any areas of the skin, including the wound areas




Genotype
MGI:3819271
cn6
Allelic
Composition
Gna11tm1Soff/Gna11tm1Soff
Gnaqtm2Soff/Gnaqtm2Soff
X/Tg(Myh11-icre/ERT2)1Soff
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gna11tm1Soff mutation (0 available); any Gna11 mutation (16 available)
Gnaqtm2Soff mutation (0 available); any Gnaq mutation (21 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• tamoxifen-treated mice exhibit decreased blood pressure following treatment with angiotensin II, vasopressin and endothelin compared to in wild-type mice
• tamoxifen-treated mice exposed to DOCA-salt do not develop hypertension and DOCA-salt treated mice exposed to tamoxifen following the onset of hypertension exhibit a drop in blood pressure compared to in similarly treated wild-type mice
• following a normal transient increase in mean arterial blood pressure upon treatment with tamoxifen, mice exhibit a drop in mean arterial blood pressure below normal levels
• slight in the absence of tamoxifen induction
• tamoxifen-treated mice fail to exhibit vasocontractile effects induced by phenylephrine or angiotensin II as do wild-type mice
• tamoxifen-treated mice exhibit reduced vasocontraction in response to serotonine, vasopressin, U46619 and endothelin-1 compared to similarly treated wild-type mice

muscle
• tamoxifen-treated mice fail to exhibit vasocontractile effects induced by phenylephrine or angiotensin II as do wild-type mice
• tamoxifen-treated mice exhibit reduced vasocontraction in response to serotonine, vasopressin, U46619 and endothelin-1 compared to similarly treated wild-type mice




Genotype
MGI:5775198
cn7
Allelic
Composition
Engtm2.1Hma/Engtm2.1Hma
Tg(Myh11-icre/ERT2)1Soff/0
Genetic
Background
involves: 129P2/OlaHsd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Engtm2.1Hma mutation (2 available); any Eng mutation (39 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• tamoxifen treated adults do not exhibit arteriovenous (AV) shunts in any areas of the skin including the wound areas




Genotype
MGI:5588166
cn8
Allelic
Composition
Ano1tm1.1Cahb/Ano1tm1.1Cahb
Tg(Myh11-icre/ERT2)1Soff/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ano1tm1.1Cahb mutation (0 available); any Ano1 mutation (35 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• tamoxifen-treated mice exhibit normal cardiac parameters (fractional shortening, cardiac output, ejection fraction, and heart rate)
• absent calcium-activated chloride currents in pericytes of small arterioles from brain, retina, skeletal muscle and skin of tamoxifen-treated mice
• almost absent U46619-induced depolarization in pericytes of tamoxifen-treated mice despite pericyte hyperpolarization after agonist application without a further increase upon replacement of chloride with methanesulfonate
• vascular smooth muscle cells lack calcium-activated chloride currents in tamoxifen-treated mice
• decreased pressure amplitude in tamoxifen-treated mice
• in tamoxifen-treated mice and more so in the presence of angiotensin II
• low-salt diet does not further decrease blood pressure
• however, systemic blood pressure differences are eliminated on a high-salt diet
• reduced brain and retina small arteriole contractility in tamoxifen-treated mice
• reduced vascular smooth muscle cell contractility in the aorta of tamoxifen-treated mice
• however, contractility in mesenteric arteries is normal

homeostasis/metabolism
N
• tamoxifen-treated mice exhibit normal plasma aldosterone, renin, angiotensin II, potassium and various blood gas parameters
• tamoxifen-treated mice exhibit normal creatinine clearance and fractional excretion of sodium, chloride and potassium

muscle
• vascular smooth muscle cells lack calcium-activated chloride currents in tamoxifen-treated mice
• reduced vascular smooth muscle cell contractility in the aorta of tamoxifen-treated mice
• however, contractility in mesenteric arteries is normal




Genotype
MGI:3819345
cn9
Allelic
Composition
Gna12tm1Citb/Gna12tm1Citb
Gna13tm2.1Soff/Gna13tm2.1Soff
X/Tg(Myh11-icre/ERT2)1Soff
Genetic
Background
involves: 129S1/Sv * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gna12tm1Citb mutation (0 available); any Gna12 mutation (14 available)
Gna13tm2.1Soff mutation (0 available); any Gna13 mutation (9 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• tamoxifen-treated mice exhibit decreased blood pressure following treatment with U46619, vasopressin and endothelin compared to in wild-type mice
• tamoxifen-treated mice exposed to DOCA-salt do not develop hypertension and DOCA-salt treated mice exposed to tamoxifen following the onset of hypertension exhibit a drop in blood pressure compared to in similarly treated wild-type mice
• tamoxifen-treated mice exhibit reduced vasocontraction in response to angiotensin II, U46619 and endothelin-1 compared to in similarly treated wild-type mice

muscle
• tamoxifen-treated mice exhibit reduced vasocontraction in response to angiotensin II, U46619 and endothelin-1 compared to in similarly treated wild-type mice




Genotype
MGI:3845037
cn10
Allelic
Composition
Kcnma1tm1Ruth/Kcnma1tm2.1Ruth
X/Tg(Myh11-icre/ERT2)1Soff
Genetic
Background
involves: 129/Sv * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kcnma1tm1Ruth mutation (0 available); any Kcnma1 mutation (60 available)
Kcnma1tm2.1Ruth mutation (0 available); any Kcnma1 mutation (60 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• the iberiotoxin sensitive component of the large noninactivating outward currents induced in urinary bladder smooth muscle cells by membrane depolarization is absent after tamoxifen treatment
• following tamoxifen treatment, peak contractions are more accentuated and maximal contraction is seen at lower electric field stimulation frequencies in detrusor muscle strips with intact urothelium
• following tamoxifen treatment, peak contractions of detrusor muscle strips with intact urothelium are stronger at stimulation frequencies of 1, 2, and 4 Hz compared to mice homozygous for Kcnma1tm1Ruth
• following tamoxifen treatment, an increase in the number of micturitions following intake of a defined amount of fluid is seen compared to both wild-type mice and mice homozygous for Kcnma1tm1Ruth

muscle
• following tamoxifen treatment, peak contractions are more accentuated and maximal contraction is seen at lower electric field stimulation frequencies in detrusor muscle strips with intact urothelium compared to wild-type controls
• following tamoxifen treatment, urinary bladder detrusor muscle is more sensitive to isoproterenol and Sp-5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole-3',5'-monophosphorothioate induced inhibition of contractility compared to controls
• following tamoxifen treatment, peak contractions of detrusor muscle strips with intact urothelium are stronger at stimulation frequencies of 1, 2, and 4 Hz compared to mice homozygous for Kcnma1tm1Ruth




Genotype
MGI:5426419
cn11
Allelic
Composition
Rgs2tm1.1Kjb/Rgs2tm1.1Kjb
X/Tg(Myh11-icre/ERT2)1Soff
Genetic
Background
involves: 129X1/SvJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rgs2tm1.1Kjb mutation (0 available); any Rgs2 mutation (14 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• treatment with tamoxifen has an insignificant affect on either acetyl choline or sodium nitroprusside induced dilation of mesenteric arteries relative to controls




Genotype
MGI:6236323
cn12
Allelic
Composition
Tg(ACTB-EGFP,-Kcnj8*G343D)9Nich/0
Tg(Myh11-icre/ERT2)1Soff/0
Genetic
Background
involves: C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(ACTB-EGFP,-Kcnj8*G343D)9Nich mutation (0 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• systolic and diastolic blood pressures are lower 3 weeks following tamoxifen induction
• however, heart rate is not affected
• in vascular smooth muscle cells (VSMC), potassium currents are higher than in control VSMCs under basal conditions and with the K(ATP) channel opener, pinacidil, indicating enhanced K(ATP) channel currents
• contraction of mesenteric arteries in response to phenylephrine is shifted about 10-fold to higher phenylephrine concentration compared to control arteries , with an even greater relative shift in the presence of pinacidil, indicating reduced contractility of blood vessels
• however, following constriction by high phenylephrine concentration, subsequent K(ATP)-independent relaxation in response to sodium nitroprusside is not different

muscle
• in vascular smooth muscle cells (VSMC), potassium currents are higher than in control VSMCs under basal conditions and with the K(ATP) channel opener, pinacidil, indicating enhanced K(ATP) channel currents
• contraction of mesenteric arteries in response to phenylephrine is shifted about 10-fold to higher phenylephrine concentration compared to control arteries , with an even greater relative shift in the presence of pinacidil, indicating reduced contractility of blood vessels
• however, following constriction by high phenylephrine concentration, subsequent K(ATP)-independent relaxation in response to sodium nitroprusside is not different




Genotype
MGI:6236322
cn13
Allelic
Composition
Tg(ACTB-EGFP,-Kcnj8)1Nich/0
Tg(Myh11-icre/ERT2)1Soff/0
Genetic
Background
involves: C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(ACTB-EGFP,-Kcnj8)1Nich mutation (0 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• systolic and diastolic blood pressures are not affected 3 weeks following tamoxifen induction




Genotype
MGI:6236324
cn14
Allelic
Composition
Tg(ACTB-EGFP,-Kcnj8*Q53R*G343D)1Nich/0
Tg(Myh11-icre/ERT2)1Soff/0
Genetic
Background
involves: C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(ACTB-EGFP,-Kcnj8*Q53R*G343D)1Nich mutation (0 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• systolic and diastolic blood pressures are lower 3 weeks following tamoxifen induction
• however, heart rate is not affected




Genotype
MGI:4442363
cn15
Allelic
Composition
Arhgef1tm1Rmt/Arhgef1tm1Rmt
X/Tg(Myh11-icre/ERT2)1Soff
Genetic
Background
involves: C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Arhgef1tm1Rmt mutation (0 available); any Arhgef1 mutation (58 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• cardiac hypertrophy, as assessed by the heart to body weight ratio, is significantly reduced in mice treated with both tamoxifen and Angiotensin II

cardiovascular system
• arterial wall remodeling in response to Angiotensin II treatment is absent
• cardiac hypertrophy, as assessed by the heart to body weight ratio, is significantly reduced in mice treated with both tamoxifen and Angiotensin II
• Angiotensin II or N-nitro-l-arginine (L-NAME) treatment do not increase blood pressure in tamoxifen treated mice
• tamoxifen treatment starting 10 days after the beginning of Angiotensin II treatment is able to reverse Angiotensin II induced hypertension
• mice treated with deoxycorticosterone acetate plus NaCl are not completely protected from induced hypertension and are resistant to the blood pressure-lowering effects of the subsequent treatment with an Angiotensin II type 1 receptor antagonist
• the amplitude of Angiotensin II induced contractions was much lower in the ex vivo aortic rings, from tamoxifen treated mice
• in tamoxifen treated mice the in vivo response to Angiotensin II is reduced

muscle
• the amplitude of Angiotensin II induced contractions was much lower in the ex vivo aortic rings, from tamoxifen treated mice
• in tamoxifen treated mice the in vivo response to Angiotensin II is reduced

homeostasis/metabolism
• N-nitro-l-arginine (L-NAME) does not induce hypertension in tamoxifen treated mice
• mice treated with deoxycorticosterone acetate plus NaCl are not completely protected from induced hypertension and are resistant to the blood pressure-lowering effects of the subsequent treatment with an Angiotensin II type 1 receptor antagonist




Genotype
MGI:5776052
cn16
Allelic
Composition
Ppp1r12aem1Sfsh/Ppp1r12a+
Tg(Myh11-icre/ERT2)1Soff/0
Genetic
Background
involves: C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ppp1r12aem1Sfsh mutation (1 available); any Ppp1r12a mutation (47 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• tamoxifen-treated mice exhibit a 5-fold increase in sensitivity to 8-Br-cGMP under calcium clamp and increased maximal relaxation in mesenteric arteries compared with control mice




Genotype
MGI:5605986
cn17
Allelic
Composition
Rgs4tm1Sdlk/Rgs4tm1Sdlk
Tg(Myh11-icre/ERT2)1Soff/?
Genetic
Background
involves: FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rgs4tm1Sdlk mutation (1 available); any Rgs4 mutation (15 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• following 25 minute bilateral ischemic kidney injury (25BI), cumulative survival is decreased as compared to controls

hematopoietic system
• increased numbers of macrophages localize to injured kidneys 18 hours after 10 minute unilateral kidney injury as compared to controls

homeostasis/metabolism
• serum creatinine levels are increased 88% 48 hours after 25BI as compared to controls

immune system
• increased numbers of macrophages localize to injured kidneys 18 hours after 10 minute unilateral kidney injury as compared to controls

cellular
• increased numbers of macrophages localize to injured kidneys 18 hours after 10 minute unilateral kidney injury as compared to controls

renal/urinary system
• tubular injury is more extensive 24 hours after 25BI as compared to controls




Genotype
MGI:6275077
cn18
Allelic
Composition
Tg(ACTB-EGFP,-Kcnj8*)1Wco/0
Tg(Myh11-icre/ERT2)1Soff/0
Genetic
Background
involves: FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(ACTB-EGFP,-Kcnj8*)1Wco mutation (0 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mice exhibit an increase in blood pressure following tamoxifen treatment





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
01/24/2023
MGI 6.22
The Jackson Laboratory