About   Help   FAQ
Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(tetO-cre)3Jig
transgene insertion 3, Jeffrey I Gordon
MGI:3041443
Summary 3 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Krastm1Bbd/Kras+
Trp53tm1Brd/Trp53+
Tg(Cela1-tTA)#Eps/?
Tg(tetO-cre)3Jig/?
involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/SvJ * FVB/N MGI:5502432
cn2
Clcn3tm1.1Jrhm/Clcn3tm1.1Jrhm
Tg(Myh6-tTA)6Smbf/0
Tg(tetO-cre)3Jig/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N MGI:5706585
cn3
Krastm1Bbd/Krastm1Bbd
Tg(Cela1-tTA)#Eps/?
Tg(tetO-cre)3Jig/?
involves: 129S1/Sv * 129X1/SvJ * FVB/N MGI:5502430


Genotype
MGI:5502432
cn1
Allelic
Composition
Krastm1Bbd/Kras+
Trp53tm1Brd/Trp53+
Tg(Cela1-tTA)#Eps/?
Tg(tetO-cre)3Jig/?
Genetic
Background
involves: 129S1/Sv * 129S7/SvEvBrd * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm1Bbd mutation (2 available); any Kras mutation (76 available)
Tg(Cela1-tTA)#Eps mutation (0 available)
Tg(tetO-cre)3Jig mutation (0 available)
Trp53tm1Brd mutation (5 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 50% mortality by 6 months of age
• 100% mortality by 1 year of age

neoplasm
• all mice develop moderately to poorly differentiated pancreatic ductal adenocarcinomas, peritoneal explants, and perineural extensions
• metastases develop affecting liver, diaphragm, lungs, lymph nodes, and spleen

endocrine/exocrine glands
• all mice develop moderately to poorly differentiated pancreatic ductal adenocarcinomas, peritoneal explants, and perineural extensions

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:119988




Genotype
MGI:5706585
cn2
Allelic
Composition
Clcn3tm1.1Jrhm/Clcn3tm1.1Jrhm
Tg(Myh6-tTA)6Smbf/0
Tg(tetO-cre)3Jig/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Clcn3tm1.1Jrhm mutation (0 available); any Clcn3 mutation (119 available)
Tg(Myh6-tTA)6Smbf mutation (4 available)
Tg(tetO-cre)3Jig mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• adult mice maintained off doxycline beyond the 3 week time point show increased mortality relative to age-matched on doxycline control mice

cardiovascular system
• at 3 weeks off doxycline, adult mice exhibit dramatically enlarged hears relative to age-matched on doxycline control mice
• at 3 weeks off doxycline, adult mice display severe signs of myocardial hypertrophy
• at 3 weeks off doxycycline, adult mice show a significantly increased heart mass and heart mass:body weight ratio relative to age-matched on doxycline control mice
• however, body weight is not significantly altered at 3 weeks off doxycycline
• at 1.5 and 3 weeks off doxycycline, adult mice display dilated cardiomyopathy (DCM), unlike age-matched on doxycline control mice
• DCM is more pronounced at 3 weeks off doxycycline
• at 3 weeks off doxycline, adult mice show significantly reduced left ventricular ejection fraction (LVEF) and fractional shortening (%FS) relative to age-matched on doxycline control mice
• M-mode echocardiography revealed a significant increase in the chamber cavity (left ventricular internal diameter, systolic [LVIDs] and LVID, diastolic [LVIDd]), left ventricular mass (LVM) and LVM/body weight ratio, and a marked decrease in LVEF and %FS in mice off doxycycline for 1.5 and 3 weeks relative to age-matched on doxycline control mice
• electrophysiological analysis of native volume-sensitive chloride channels (VSOACs) in isolated atrial and ventricular myocytes 3 weeks off doxycycline revealed a complete elimination of hypotonic-induced VSOAC currents, whereas at 1.5 weeks, VSOAC current densities are significantly reduced, relative to age-matched on doxycycline controls; no difference in current densities are noted under isotonic conditions prior to cell swelling
• membrane capacitance is significantly increased in ventricular myocytes from mice 3 weeks off doxyclycline relative to ventricular myocytes from on doxycycline control mice; however, no difference in membrane capacitance is noted in atrial myocytes at 3 weeks off doxycycline
• at 1.5 weeks off doxycycline, residual hypotonic-induced VSOAC currents are totally abolished in isolated atrial myocytes by perfusion of 100 nM PDBu (a protein kinase C activator), similar to VSOAC currents in atrial cells from on doxycycline control mice
• at 3 weeks off doxycline, adult mice display severe signs of heart failure

muscle
• at 3 weeks off doxycline, adult mice display severe signs of myocardial hypertrophy
• at 1.5 and 3 weeks off doxycycline, adult mice display dilated cardiomyopathy (DCM), unlike age-matched on doxycline control mice
• DCM is more pronounced at 3 weeks off doxycycline
• at 3 weeks off doxycline, adult mice show significantly reduced left ventricular ejection fraction (LVEF) and fractional shortening (%FS) relative to age-matched on doxycline control mice

growth/size/body
• at 3 weeks off doxycline, adult mice exhibit dramatically enlarged hears relative to age-matched on doxycline control mice
• at 3 weeks off doxycline, adult mice display severe signs of myocardial hypertrophy
• at 3 weeks off doxycycline, adult mice show a significantly increased heart mass and heart mass:body weight ratio relative to age-matched on doxycline control mice
• however, body weight is not significantly altered at 3 weeks off doxycycline




Genotype
MGI:5502430
cn3
Allelic
Composition
Krastm1Bbd/Krastm1Bbd
Tg(Cela1-tTA)#Eps/?
Tg(tetO-cre)3Jig/?
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm1Bbd mutation (2 available); any Kras mutation (76 available)
Tg(Cela1-tTA)#Eps mutation (0 available)
Tg(tetO-cre)3Jig mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• focal morphological lesions develop in acinar and centroacinar cells at 1-3 months
• acinar to ductal metaplasias develop
• some mice develop ductal adenocarcinomas by 12 months
• properties are similar to those in human patients
• sometimes areas of non malignant hyperplasia develop
• latency is increased if gene expression is delayed by maintaining exposure to doxycycline until 10 days of age
• if doxycycline exposure continues to 2 months of age, no pancreatic abnormalities develop

endocrine/exocrine glands
• focal morphological lesions develop in acinar and centroacinar cells at 1-3 months
• acinar to ductal metaplasias develop
• some mice develop ductal adenocarcinomas by 12 months
• properties are similar to those in human patients
• sometimes areas of non malignant hyperplasia develop

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:119988





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)
Citing These Resources
Funding Information
Warranty Disclaimer, Privacy Notice, Licensing, & Copyright
Send questions and comments to User Support.
last database update
04/09/2024
MGI 6.23
The Jackson Laboratory