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Phenotypes Associated with This Genotype
Genotype
MGI:3771372
Allelic
Composition
Stat1tm1Rds/Stat1tm1Rds
Genetic
Background
129S6/SvEv-Stat1tm1Rds/Tac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Stat1tm1Rds mutation (4 available); any Stat1 mutation (24 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• 65% of nulliparous mice develop spontaneous mammary adenocarcinomas with a median tumor onset of 23 months
• 91% of multiparous mice develop mammary tumors with a median tumor onset of 14.8 months of age
• mammary tumors are estrogen receptor-alpha and progesterone receptor positive and HER2 negative and display display a surface marker phenotype reflective of luminal mammary tumors
• early lesions vary from distended ducts to small cystically dilated clusters of alveoli and contain atypical cells indicative of mammary intraepithelial neoplasia
• some tumors have invasive nests of neoplastic cells with areas of fibrosis and inflammation

homeostasis/metabolism
• following exposure to ischemia/reperfusion
• unlike wild-type cells, primary neurons are resistant to interferon-gamma-induced neurotoxicity
• treatment with LPS and DGalN fail to induce an increase in serum interferon-gamma levels as in wild-type mice
• unlike in wild-type mice, treatment with LPS and DGalN or TNF-alpha and interferon-gamma fails to increase nitric oxide levels

integument
• 65% of nulliparous mice develop spontaneous mammary adenocarcinomas with a median tumor onset of 23 months
• 91% of multiparous mice develop mammary tumors with a median tumor onset of 14.8 months of age
• mammary tumors are estrogen receptor-alpha and progesterone receptor positive and HER2 negative and display display a surface marker phenotype reflective of luminal mammary tumors
• early lesions vary from distended ducts to small cystically dilated clusters of alveoli and contain atypical cells indicative of mammary intraepithelial neoplasia
• some tumors have invasive nests of neoplastic cells with areas of fibrosis and inflammation

cardiovascular system
• following exposure to ischemia/reperfusion
• following exposure to ischemia/reperfusion

nervous system
• unlike wild-type cells, primary neurons are resistant to interferon-gamma-induced neurotoxicity

neoplasm
• 65% of nulliparous mice develop spontaneous mammary adenocarcinomas with a median tumor onset of 23 months
• 91% of multiparous mice develop mammary tumors with a median tumor onset of 14.8 months of age
• mammary tumors are estrogen receptor-alpha and progesterone receptor positive and HER2 negative and display display a surface marker phenotype reflective of luminal mammary tumors
• early lesions vary from distended ducts to small cystically dilated clusters of alveoli and contain atypical cells indicative of mammary intraepithelial neoplasia
• some tumors have invasive nests of neoplastic cells with areas of fibrosis and inflammation

muscle
• following exposure to ischemia/reperfusion

cellular
• following exposure to ischemia/reperfusion
• unlike wild-type cells, primary neurons are resistant to interferon-gamma-induced neurotoxicity
• unlike in wild-type mice, treatment with LPS and DGalN or TNF-alpha and interferon-gamma fails to increase hepatocyte apoptosis
• inhibition of RANKL induced osteoclastogenesis by flagellin and lipopolysaccharide is reversed
• unlike in wild-type mice, treatment with LPS and DGalN or TNF-alpha and interferon-gamma fails to increase the production of reactive oxygen species in hepatocytes

immune system
• inhibition of RANKL induced osteoclastogenesis by flagellin and lipopolysaccharide is reversed
• unlike in wild-type mice, treatment with LPS and DGalN fails to decrease K T cell numbers
• macrophages exhibit impaired ability to kill Bacillus anthracis compared with wild-type cells
• treatment with LPS and DGalN fail to induce an increase in serum interferon-gamma levels as in wild-type mice
• following exposure of macrophages to LPS or Bacillus anthracis spores

hematopoietic system
• inhibition of RANKL induced osteoclastogenesis by flagellin and lipopolysaccharide is reversed
• unlike in wild-type mice, treatment with LPS and DGalN fails to decrease K T cell numbers
• macrophages exhibit impaired ability to kill Bacillus anthracis compared with wild-type cells

skeleton
• inhibition of RANKL induced osteoclastogenesis by flagellin and lipopolysaccharide is reversed

liver/biliary system
• unlike in wild-type mice, treatment with LPS and DGalN or TNF-alpha and interferon-gamma fails to increase hepatocyte apoptosis

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
breast cancer DOID:1612 OMIM:114480
J:216040


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
11/12/2019
MGI 6.14
The Jackson Laboratory