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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Trim29tm1c(EUCOMM)Wtsi
targeted mutation 1c, Wellcome Trust Sanger Institute
MGI:7608151
Summary 5 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
Trim29tm1c(EUCOMM)Wtsi/Trim29tm1c(EUCOMM)Wtsi
Trp53tm1Brn/Trp53+
involves: 129 * C57BL/6 * CBA MGI:7736726
cn2
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Tg(Pdx1-cre)89.1Dam/0
Trim29tm1c(EUCOMM)Wtsi/Trim29tm1c(EUCOMM)Wtsi
involves: 129 * C57BL/6 * CBA MGI:7736742
cn3
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
Trim29tm1c(EUCOMM)Wtsi/Trim29tm1c(EUCOMM)Wtsi
involves: 129 * C57BL/6 * CBA MGI:7736747
cn4
Trim29tm1c(EUCOMM)Wtsi/Trim29tm1c(EUCOMM)Wtsi
Tg(Myh6-cre)2182Mds/0
involves: C57BL/6J * C57BL/6N * C57BL/6NTac MGI:7662823
cn5
Trim29tm1c(EUCOMM)Wtsi/Trim29tm1c(EUCOMM)Wtsi
Tg(Pdx1-cre)6Tuv/0
involves: C57BL/6N * FVB/N MGI:7736562


Genotype
MGI:7736726
cn1
Allelic
Composition
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
Trim29tm1c(EUCOMM)Wtsi/Trim29tm1c(EUCOMM)Wtsi
Trp53tm1Brn/Trp53+
Genetic
Background
involves: 129 * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(EYFP)Cos mutation (11 available); any Gt(ROSA)26Sor mutation (994 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trim29tm1c(EUCOMM)Wtsi mutation (0 available); any Trim29 mutation (28 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
N
• 73.3% of 3-month old and 75% of 12-month old mice show normal pancreas
• although 26.7% of 3-month old and 25% of 12-month old mice show rare acinar-ductal metaplasia and low-grade pancreatic intraepithelial neoplasia (PanIN1) lesions, these lesions express TRIM29 due to incomplete recombination of the floxed allele

mortality/aging
N
• all mice are alive at 12 months




Genotype
MGI:7736742
cn2
Allelic
Composition
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Tg(Pdx1-cre)89.1Dam/0
Trim29tm1c(EUCOMM)Wtsi/Trim29tm1c(EUCOMM)Wtsi
Genetic
Background
involves: 129 * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(EYFP)Cos mutation (11 available); any Gt(ROSA)26Sor mutation (994 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trim29tm1c(EUCOMM)Wtsi mutation (0 available); any Trim29 mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
N
• mice with cerulein-induced acute pancreatitis show reversion of acinar-ductal metaplasia lesions to normal acinar morphology after 7 days of recovery similarly as in wild-type mice




Genotype
MGI:7736747
cn3
Allelic
Composition
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
Trim29tm1c(EUCOMM)Wtsi/Trim29tm1c(EUCOMM)Wtsi
Genetic
Background
involves: 129 * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(EYFP)Cos mutation (11 available); any Gt(ROSA)26Sor mutation (994 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trim29tm1c(EUCOMM)Wtsi mutation (0 available); any Trim29 mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
N
• mice with cerulein-induced acute pancreatitis show reversion of acinar-ductal metaplasia lesions to normal acinar morphology after 7 days of recovery as in wild-type mice
• primary pancreatic acinar cells from 1.5-month-old mice grown in 3D collagen culture show attenuated KRAStm4Tyj-induced acinar cell transdifferentiation and acinar-ductal metaplasia formation

neoplasm
• primary pancreatic acinar cells from 1.5-month-old mice grown in 3D collagen culture show attenuated KRAStm4Tyj-induced acinar cell transdifferentiation and acinar-ductal metaplasia formation




Genotype
MGI:7662823
cn4
Allelic
Composition
Trim29tm1c(EUCOMM)Wtsi/Trim29tm1c(EUCOMM)Wtsi
Tg(Myh6-cre)2182Mds/0
Genetic
Background
involves: C57BL/6J * C57BL/6N * C57BL/6NTac
Cell Lines EPD0439_4_D01
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Myh6-cre)2182Mds mutation (3 available)
Trim29tm1c(EUCOMM)Wtsi mutation (0 available); any Trim29 mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• following i.p. infection with Coxsackievirus B3 (CVB3, strain Nancy), mice show significantly improved survival rates relative to CVB3-infected controls

immune system
• when myeloid-derived suppressor cells (MDSCs) from 3-day CVB3-infected hearts are cocultured with negatively selected CD3+ T cells and stimulated with anti-CD3 and anti-CD28 antibodies, the % of proliferating CD8+ T cells is significantly higher than that in controls
• following CVB3 infection, mice show significantly higher IFN-alpha and IFN-beta levels in the heart than CVB3-infected controls
• following CVB3 infection, mice show significantly lower IL-6 and IL-1beta levels in the heart than CVB3-infected controls
• following CVB3 infection, mice show significantly lower TNF levels in the heart than CVB3-infected controls
• upon in vitro stimulation with PMA/ionomycin, CD8+ T cells show a significantly enhanced IFN-gamma producing ability in the heart and spleen from 2-day CVB3-infected mice
• however, the IFN-gamma-producing ability of CD8+ T cells in spleen is similar to that in untreated controls before CVB3 infection
• 2 days after CVB3 infection, mice show significantly lower cell numbers of monocytic MDSCs (CD11b+Ly6C+Ly6G-), macrophages, neutrophils, B cells and T cells infiltrated in the heart than CVB3-infected controls
• following i.p. infection with Coxsackievirus B3 (CVB3, strain Nancy), mice show significantly less inflammation and infiltration of inflammatory cells in heart, lower heart weight/baseline body weight, improved cardiac function (as assessed by ejection fraction and fractional shortening), reduced viral titers in heart, pancreas and spleen homogenates, and lower levels of cardiac inflammatory cytokines (IL-6, IL-1beta, and TNF) than CVB3-infected controls, indicating protection from viral myocarditis
• following i.p. infection with Coxsackievirus B3 (CVB3, strain Nancy), mice show significantly improved survival rates relative to CVB3-infected controls

cellular
• in vitro, primary neonatal cardiomyocytes infected with CVB3 show dramatically reduced expression of CHOP, cleaved caspase-3, and BAX, indicating reduced EIF2AK3-mediated ER stress and apoptosis
• when myeloid-derived suppressor cells (MDSCs) from 3-day CVB3-infected hearts are cocultured with negatively selected CD3+ T cells and stimulated with anti-CD3 and anti-CD28 antibodies, the % of proliferating CD8+ T cells is significantly higher than that in controls
• following infection with CVB3, primary neonatal cardiomyocytes from 2-day-old mice show dramatically reduced phosphorylation of EIF2AK3 (eukaryotic translation initiation factor 2 alpha kinase 3, also known as PERK), suggesting reduced EIF2AK3-mediated ER stress

homeostasis/metabolism
• following CVB3 infection, mice show dramatically reduced circulating creatine kinase levels relative to CVB3-infected controls
• following CVB3 infection, mice show significantly higher IFN-alpha and IFN-beta levels in the heart than CVB3-infected controls
• following CVB3 infection, mice show significantly lower IL-6 and IL-1beta levels in the heart than CVB3-infected controls
• following CVB3 infection, mice show significantly lower TNF levels in the heart than CVB3-infected controls

hematopoietic system
• when myeloid-derived suppressor cells (MDSCs) from 3-day CVB3-infected hearts are cocultured with negatively selected CD3+ T cells and stimulated with anti-CD3 and anti-CD28 antibodies, the % of proliferating CD8+ T cells is significantly higher than that in controls
• 2 days after CVB3 infection, mice show a significantly lower frequency of myeloid-derived suppressor cells (CD11b+ Gr1+ MDSCs) in the heart and spleen than CVB3-infected controls
• however, the frequency of MDSCs in spleen is similar to that in untreated controls before CVB3 infection

cardiovascular system
• in vitro, primary neonatal cardiomyocytes infected with CVB3 show dramatically reduced expression of CHOP, cleaved caspase-3, and BAX, indicating reduced EIF2AK3-mediated ER stress and apoptosis

muscle
• in vitro, primary neonatal cardiomyocytes infected with CVB3 show dramatically reduced expression of CHOP, cleaved caspase-3, and BAX, indicating reduced EIF2AK3-mediated ER stress and apoptosis




Genotype
MGI:7736562
cn5
Allelic
Composition
Trim29tm1c(EUCOMM)Wtsi/Trim29tm1c(EUCOMM)Wtsi
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: C57BL/6N * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trim29tm1c(EUCOMM)Wtsi mutation (0 available); any Trim29 mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
N
• mice show normal pancreatic weight, morphology, and histology up to 12 months of age

mortality/aging
N
• mice are born at the expected frequency





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last database update
12/17/2024
MGI 6.24
The Jackson Laboratory