All Phenotypes Trim29<tm1a(EUCOMM)Wtsi> MGI Mouse

decreased susceptibility to Picornaviridae infection induced morbidity/mortality ( J:349246 )

• following i.p. infection with Coxsackievirus B3 (CVB3, strain Nancy), mice show significantly improved survival rates relative to CVB3-infected wild-type controls

increased interferon level ( J:349246 )

• following CVB3 infection, mice show significantly higher IFN-alpha and IFN-beta levels in the heart than CVB3-infected wild-type controls

decreased interleukin level ( J:349246 )

• following CVB3 infection, mice show significantly lower IL-6 and IL-1beta levels in the heart than CVB3-infected wild-type controls

abnormal tumor necrosis factor level ( J:349246 )

• following CVB3 infection, mice show significantly lower TNF levels in the heart than CVB3-infected wild-type controls

abnormal interferon secretion ( J:349246 )

• in vitro, primary neonatal cardiomyocytes infected with CVB3 or EMCV show significantly increased production of type I interferons to restrict cardiotropic viruses by relieving ROS-mediated TBK1 inhibition

increased interferon-alpha secretion ( J:349246 )

• in vitro, primary neonatal cardiomyocytes infected with CVB3 or EMCV exhibit significantly increased IFN-alpha production relative to similarly infected wild-type cardiomyocytes

increased interferon-beta secretion ( J:349246 )

• in vitro, primary neonatal cardiomyocytes infected with CVB3 or EMCV exhibit significantly increased IFN-beta production relative to similarly infected wild-type cardiomyocytes

decreased susceptibility to Picornaviridae infection ( J:349246 )

• following i.p. infection with Coxsackievirus B3 (CVB3, strain Nancy), mice show significantly less inflammation and infiltration of inflammatory cells in heart and pancreas, 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 wild-type controls, indicating protection from viral myocarditis

decreased susceptibility to Picornaviridae infection induced morbidity/mortality ( J:349246 )

• following i.p. infection with Coxsackievirus B3 (CVB3, strain Nancy), mice show significantly improved survival rates relative to CVB3-infected wild-type controls

decreased fetal cardiomyocyte apoptosis ( J:349246 )

• in vitro, primary neonatal cardiomyocytes infected with CVB3 or EMCV show significantly reduced mRNA levels of the EIF2AK3-regulated transcription factors Atf4 and Chop and the downstream apoptosis-associated regulators Bim, Noxa and Puma

• neonatal cardiomyocytes infected with CVB3 or EMCV show increased cell viability with significantly decreased expression of CHOP, cleaved caspase-3, BAX and ANP and increased expression of the antiapoptotic protein BCL-2, indicating reduced EIF2AK3-mediated ER stress and apoptosis

decreased endoplasmic reticulum stress ( J:349246 )

• following infection with CVB3 or EMCV, primary neonatal cardiomyocytes from 2-day-old mice show a drastic reduction in expression and activated phosphorylation of EIF2AK3 (eukaryotic translation initiation factor 2 alpha kinase 3, also known as PERK), suggesting reduced EIF2AK3-mediated ER stress

abnormal redox activity ( J:349246 )

• in vitro, primary neonatal cardiomyocytes infected with CVB3 or EMCV show a significant reduction in reactive oxygen species (ROS) levels relative to similarly infected wild-type cardiomyocytes

decreased circulating creatine kinase level ( J:349246 )

• following CVB3 infection, mice show dramatically reduced serum creatine kinase levels relative to CVB3-infected wild-type controls

increased interferon level ( J:349246 )

• following CVB3 infection, mice show significantly higher IFN-alpha and IFN-beta levels in the heart than CVB3-infected wild-type controls

decreased interleukin level ( J:349246 )

• following CVB3 infection, mice show significantly lower IL-6 and IL-1beta levels in the heart than CVB3-infected wild-type controls

abnormal tumor necrosis factor level ( J:349246 )

• following CVB3 infection, mice show significantly lower TNF levels in the heart than CVB3-infected wild-type controls

decreased fetal cardiomyocyte apoptosis ( J:349246 )

• in vitro, primary neonatal cardiomyocytes infected with CVB3 or EMCV show significantly reduced mRNA levels of the EIF2AK3-regulated transcription factors Atf4 and Chop and the downstream apoptosis-associated regulators Bim, Noxa and Puma

• neonatal cardiomyocytes infected with CVB3 or EMCV show increased cell viability with significantly decreased expression of CHOP, cleaved caspase-3, BAX and ANP and increased expression of the antiapoptotic protein BCL-2, indicating reduced EIF2AK3-mediated ER stress and apoptosis

decreased fetal cardiomyocyte apoptosis ( J:349246 )

• in vitro, primary neonatal cardiomyocytes infected with CVB3 or EMCV show significantly reduced mRNA levels of the EIF2AK3-regulated transcription factors Atf4 and Chop and the downstream apoptosis-associated regulators Bim, Noxa and Puma

• neonatal cardiomyocytes infected with CVB3 or EMCV show increased cell viability with significantly decreased expression of CHOP, cleaved caspase-3, BAX and ANP and increased expression of the antiapoptotic protein BCL-2, indicating reduced EIF2AK3-mediated ER stress and apoptosis

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

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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