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Phenotypes Associated with This Genotype
Genotype
MGI:2681522
Allelic
Composition
Artm1Ska/Y
Tg(CMV-cre)1Ipc/?
Genetic
Background
involves: C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Artm1Ska mutation (0 available); any Ar mutation (22 available)
Tg(CMV-cre)1Ipc mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue
• wet weights of subcutaneous, infrarenal and intraperitoneal white adipose tissues are significantly increased by 30 weeks of age
• serum lipid parameters and food intake remain unaffected

endocrine/exocrine glands
• inguinal testes
• small degenerating testes

growth/size/body
• after 10 weeks of age, the growth of males increased dramatically
• by 12 weeks of age, the body weights of mutant males are higher than those of wild-type males
• by 30 weeks of age males are obese
• growth retardation in males through 10 weeks of age

renal/urinary system
• clitoris-like phallus instead of a penis and scrotum

reproductive system
• inguinal testes
• small degenerating testes
• clitoris-like phallus instead of a penis and scrotum
• vagina with a blind end
• feminization of external appearance, including a blind vagina and a clitoris-like phallus, with absence of internal male and female reproductive organs, except for atrophic testes
• no ovaries or uteri are observed
• lower levels of androgens
• estradiol levels typical for a male

cardiovascular system
• in response to angiotensin-II stimulation, male homozygotes show a smaller increase in the cross-sectional area of cardiomyocytes relative to wild-type males
• after 6 weeks of age, male homozygotes show a significantly reduced cross-sectional area of cardiomyocytes in LV tissues relative to wild-type males
• after 6 weeks of age, male homozygotes exhibit a cardiac size reduction relative to wild-type males
• in response to angiotensin-II stimulation, male homozygotes show a smaller increase in cardiac size relative to wild-type males
• male homozygotes display no significant differences in basal levels of systolic blood pressure and heart rate; however, after 6 weeks of age, male homozygotes show a significant reduction in HW/BW ratio relative to wild-type males
• in response to angiotensin-II stimulation, male homozygotes display a smaller increase in HW/BW ratio relative to wild-type males
• in response to angiotensin-II stimulation, male homozygotes exhibit an impaired hypertrophic response with lower cardiac LV volumes that is partly associated with reduced activation of mitogen-activated protein kinases 1/2 and 5
• after 6 weeks of age, male homozygotes display a reduced LV volume relative to wild-type males
• after 6 weeks of age, male homozygotes exhibit a reduced left ventricular (LV) wall thickness relative to wild-type males
• in response to angiotensin-II stimulation, male homozygotes show a lower increase in LV wall thickening relative to wild-type males
• in response to angiotensin-II stimulation, 25-wk-old male homozygotes display an exacerbated interstitial fibrosis in the left ventricular area relative to age-matched wild-type males
• enhanced angiotensin-II-mediated cardiac interstitial fibrosis is associated with up-regulation of collagen I and III gene expression and enhanced cardiac transforming growth factor-beta1 and Smad2 activation
• at 25 weeks, male homozygotes exhibit a normal left ventricular fractional shortening (a marker of systolic function) relative to wild-type males
• however, in response to angiotensin-II stimulation, male homozygotes display a significantly attenuated LV systolic function relative to wild-type males

muscle
• in response to angiotensin-II stimulation, male homozygotes show a smaller increase in the cross-sectional area of cardiomyocytes relative to wild-type males
• after 6 weeks of age, male homozygotes show a significantly reduced cross-sectional area of cardiomyocytes in LV tissues relative to wild-type males
• at 25 weeks, male homozygotes exhibit a normal left ventricular fractional shortening (a marker of systolic function) relative to wild-type males
• however, in response to angiotensin-II stimulation, male homozygotes display a significantly attenuated LV systolic function relative to wild-type males

cellular
• in response to angiotensin-II stimulation, 25-wk-old male homozygotes display an exacerbated interstitial fibrosis in the left ventricular area relative to age-matched wild-type males
• enhanced angiotensin-II-mediated cardiac interstitial fibrosis is associated with up-regulation of collagen I and III gene expression and enhanced cardiac transforming growth factor-beta1 and Smad2 activation

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
androgen insensitivity syndrome DOID:4674 OMIM:300068
J:85484
obesity DOID:9970 OMIM:601665
J:85484


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
03/12/2024
MGI 6.23
The Jackson Laboratory