Phenotypes associated with this allele

• Allele Symbol: Cst3^tm1Karl
• Allele Name: targeted mutation 1, S Karlsson
• Allele ID: MGI:2182140
• Summary: 3 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Cst3^tm1Karl/Cst3^tm1Karl	involves: 129S/SvEv * C57BL/6	MGI:3621900
hm2	Cst3^tm1Karl/Cst3^tm1Karl	involves: 129S/SvEv * C57BL/6J * CBA	MGI:3621825
cx3	Apoe^tm1Unc/Apoe^tm1Unc Cst3^tm1Karl/Cst3^tm1Karl	involves: 129S/SvEv * C57BL/6	MGI:3621887

Genotype
MGI:3621900

hm1

• Allelic Composition: Cst3^tm1Karl/Cst3^tm1Karl
• Genetic Background: involves: 129S/SvEv * C57BL/6

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

neoplasm

increased metastatic potential ( J:62407 )

• after intravenous injection of melanoma cells, Cst3 knockout mice have 7 times fewer metastatic lung colonies than wild-type mice two weeks post injection

• null mice analyzed at times from 15 mnutes to 96 hours post-injection showed fewer melanoma cells as short a time as 1 minutes after injection compared to wild-type; at all time points, nulls showed fewer metatatic colonies/cells than wild-type mice; two weeks after injection, null mice had fewer melanoma colonies spread throughout their lungs than wild-type62407

Genotype
MGI:3621825

hm2

• Allelic Composition: Cst3^tm1Karl/Cst3^tm1Karl
• Genetic Background: involves: 129S/SvEv * C57BL/6J * CBA

nervous system

decreased susceptibility to ischemic brain injury ( J:93568 )

• in knockouts there is less neuronal damage in the cortex and striatum than in wild-type

increased cerebral infarct size ( J:93568 )

• in knockout mice the infarct volume after 40 minutes of MCA occlusion is significantly larger than in wild-type

loss of hippocampal neurons ( J:93568 )

• global ischemia of 12 minutes caused significantly less neuronal damage in the CA3 region and dentate gyrus of knockout mice than in wild-type

homeostasis/metabolism

decreased susceptibility to ischemic brain injury ( J:93568 )

• in knockouts there is less neuronal damage in the cortex and striatum than in wild-type

increased cerebral infarct size ( J:93568 )

• in knockout mice the infarct volume after 40 minutes of MCA occlusion is significantly larger than in wild-type

Genotype
MGI:3621887

cx3

• Allelic Composition: Apoe^tm1Unc/Apoe^tm1Unc; Cst3^tm1Karl/Cst3^tm1Karl
• Genetic Background: involves: 129S/SvEv * C57BL/6

homeostasis/metabolism

abnormal enzyme/coenzyme level ( J:106879 )

• aortic tissue extracts from double knockouts show higher levels of cathepsins S and L and the long form of cathepsin B than ApoE null controls

abnormal enzyme/coenzyme activity ( J:106879 )

• aortic smooth muscle cells exhibit an augmented ability to degrade elastin in vitro

cardiovascular system

abnormal aorta tunica media morphology ( J:106879 )

• double knockout mice display thinning of the tunica media in the aortic arch compared to ApoE knockouts

abnormal aorta elastic tissue morphology ( J:106879 )

• double knockouts show more framentation of elastic laminae than in either the ApoE or Cst3 single knockout mouse

abnormal aortic arch morphology ( J:106879 )

• double knockout mice display thinning of the tunica media in the aortic arch compared to ApoE knockouts

atherosclerotic lesions ( J:106879 )

• atherosclerotic lesions from aortas of double knockouts had increased smooth muscle cell content (9.3% vs. 4.2% positive lesion area) and collagen (14.4% vs. 4.6%) compared to ApoE knockout mice; fibrous caps develop significantly more in double mutants than controls

vascular smooth muscle hyperplasia ( J:106879 )

• in vitro double knockout smooth muscle cells proliferate more rapidly than control cells which might contribute to the increase in SMC and collagen content in aortic lesions

muscle

vascular smooth muscle hyperplasia ( J:106879 )

• in vitro double knockout smooth muscle cells proliferate more rapidly than control cells which might contribute to the increase in SMC and collagen content in aortic lesions