All Phenotypes Ctss<tm1Hap> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Ctss^tm1Hap/Ctss^tm1Hap	B6.129S2-Ctss^tm1Hap	MGI:3573791
cx2	Ctss^tm1Hap/Ctss^tm1Hap Ldlr^tm1Her/Ldlr^tm1Her	B6.129S-Ctss^tm1Hap Ldlr^tm1Her	MGI:5008733
cx3	Ctss^tm1Hap/Ctss^tm1Hap Dmd^mdx/Dmd^mdx	involves: 129S2/SvPas * C57BL/10ScSn	MGI:5779560
cx4	Ctss^tm1Hap/Ctss^tm1Hap Tg(Scgb1a1-rtTA,tetO-Ifng)14Eli/0	involves: 129S2/SvPas * C57BL/6 * CBA	MGI:5008742

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

immune system

abnormal T cell physiology ( J:96401 )

• very weak in vitro T cell proliferative responses to either whole AChR protein or peptides, indicating the supporting T cell repertoire never fully developed

abnormal professional antigen presenting cell physiology ( J:96401 )

• purified splenocyte antigen presenting cells were impaired in their ability to stimulate highly primed wildtype CD4+ T cells in vitro with AChR protein, indicating impaired Ag presentation

abnormal B cell physiology ( J:96401 )

• reduced B cell responses to acetylcholine receptor

• despite repeated immunization of homozygous null mice with AChR protein, there was little B cell expansion

decreased IgG level ( J:96401 )

• reduced anti-AChR IgG1, IgG2b, IgG2c subclass production in AChR-immunized homozygotes

decreased IgM level ( J:96401 )

• reduced anti-AChR IgM production in AChR-immunized homozygotes

abnormal humoral immune response ( J:96401 )

• reduced humoral responses in AChR immunized homozygotes

abnormal cytokine secretion ( J:96401 )

• production of IFN-gamma was suppressed in lymph node cells from AChR immunized homozygotes that were stimulated in vitro with AChR protein or peptides

abnormal interleukin secretion ( J:96401 )

• production of IL-2 and IL-10 was suppressed in lymph node cells from AChR immunized homozygotes that were stimulated in vitro with AChR protein or peptides

decreased susceptibility to experimental autoimmune myasthenia gravis ( J:96401 )

• homozygous null mice were markedly resistant to the development of experimental autoimmune myasthenia gravis (EAMG) (induced by acetylcholine receptor (AChR) immunization), with 17% of nulls developing EAMG compared to 75% of wildtype, and had significantly higher functional muscle acetylcholine receptors

cardiovascular system

decreased angiogenesis ( J:109410 )

• during wound healing, microvessel development is impaired compared to in wild-type mice

abnormal vascular endothelial cell physiology ( J:109410 )

• endothelial cells exhibit impaired matrigel and collagen gel invasion compared with wild-type cells

hematopoietic system

abnormal B cell physiology ( J:96401 )

• reduced B cell responses to acetylcholine receptor

• despite repeated immunization of homozygous null mice with AChR protein, there was little B cell expansion

decreased IgG level ( J:96401 )

• reduced anti-AChR IgG1, IgG2b, IgG2c subclass production in AChR-immunized homozygotes

decreased IgM level ( J:96401 )

• reduced anti-AChR IgM production in AChR-immunized homozygotes

abnormal T cell physiology ( J:96401 )

• very weak in vitro T cell proliferative responses to either whole AChR protein or peptides, indicating the supporting T cell repertoire never fully developed

Allelic Composition	Ctss^tm1Hap/Ctss^tm1Hap Ldlr^tm1Her/Ldlr^tm1Her
Genetic Background	B6.129S-Ctss^tm1Hap Ldlr^tm1Her

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctss^tm1Hap mutation (3 available); any Ctss mutation (30 available)
Ldlr^tm1Her mutation (19 available); any Ldlr mutation (76 available)

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

cardiovascular system

decreased susceptibility to atherosclerosis ( J:82520 )

• after 12 and 26 weeks on an atherogenic diet with decreased macrophage, leukocyte, and CD4+ T cells within lesions

vascular smooth muscle hypoplasia ( J:82520 )

immune system

abnormal leukocyte migration ( J:82520 )

• leukocytes exhibit impaired leukocyte transmigration compared with wild-type cells

homeostasis/metabolism

decreased circulating cholesterol level ( J:82520 )

• when fed standard chow

decreased circulating LDL cholesterol level ( J:82520 )

• when fed standard chow

muscle

vascular smooth muscle hypoplasia ( J:82520 )

cellular

abnormal leukocyte migration ( J:82520 )

• leukocytes exhibit impaired leukocyte transmigration compared with wild-type cells

hematopoietic system

abnormal leukocyte migration ( J:82520 )

• leukocytes exhibit impaired leukocyte transmigration compared with wild-type cells

Allelic Composition	Ctss^tm1Hap/Ctss^tm1Hap Dmd^mdx/Dmd^mdx
Genetic Background	involves: 129S2/SvPas * C57BL/10ScSn

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctss^tm1Hap mutation (3 available); any Ctss mutation (30 available)
Dmd^mdx mutation (30 available); any Dmd mutation (153 available)

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

behavior/neurological

impaired exercise endurance ( J:230788 )

• treadmill running time is decreased as compared to wild-type, but increased as compared to homozygous Dmd^mdx mice

homeostasis/metabolism

impaired exercise endurance ( J:230788 )

• treadmill running time is decreased as compared to wild-type, but increased as compared to homozygous Dmd^mdx mice

increased circulating creatine kinase level ( J:230788 )

• increase in serum creatine kinase levels as compared to wild-type, but decreased as compared to homozygous Dmd^mdx mic

muscle

abnormal skeletal muscle fiber morphology ( J:230788 )

• decreased membrane stability as compared to wild-type, but increased as compared to homozygous Dmd^mdx mice

skeletal muscle fiber necrosis ( J:230788 )

• myofiber necrosis is increased as compared to wild-type, but decreased as compared to homozygous Dmd^mdx mic

centrally nucleated skeletal muscle fibers ( J:230788 )

• increase in central nucleation at 2 and 10 months of age as compared to wild-type, but decreased as compared to homozygous Dmd^mdx mice

skeletal muscle fibrosis ( J:230788 )

• fibrosis at 2 months and 10 months is increased as compared to wild-type, but decreased as compared to homozygous Dmd^mdx mice

dystrophic muscle ( J:230788 )

• increased as compared to wild-type, but decreased as compared to homozygous Dmd^mdx mice

cellular

skeletal muscle fiber necrosis ( J:230788 )

• myofiber necrosis is increased as compared to wild-type, but decreased as compared to homozygous Dmd^mdx mic

Allelic Composition	Ctss^tm1Hap/Ctss^tm1Hap Tg(Scgb1a1-rtTA,tetO-Ifng)14Eli/0
Genetic Background	involves: 129S2/SvPas * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctss^tm1Hap mutation (3 available); any Ctss mutation (30 available)
Tg(Scgb1a1-rtTA,tetO-Ifng)14Eli mutation (0 available)

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

respiratory system

emphysema ( J:100854 )

• following treatment with doxycycline but not as much as in Tg(Scgb1a1-rtTA,tetO-Ifng)14Eli mice

abnormal lung volume ( J:100854 )

• doxycycline-treated mice exhibit increased lung volume compared to in wild-type mice but not as much as in Tg(Scgb1a1-rtTA,tetO-Ifng)14Eli mice

increased lung compliance ( J:100854 )

• following treatment with doxycycline but not as much as in Tg(Scgb1a1-rtTA,tetO-Ifng)14Eli mice

immune system

increased neutrophil cell number ( J:100854 )