Phenotypes associated with this allele

• Allele Symbol: Camk2g^tm1.1Irt
• Allele Name: targeted mutation 1.1, Ira Tabas
• Allele ID: MGI:4398829
• Summary: 2 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Camk2g^tm1.1Irt/Camk2g^tm1.1Irt	involves: C57BL/6 * C57BL/6J	MGI:4398843
hm2	Camk2g^tm1.1Irt/Camk2g^tm1.1Irt	involves: C57BL/6J	MGI:5927424

Genotype
MGI:4398843

hm1

• Allelic Composition: Camk2g^tm1.1Irt/Camk2g^tm1.1Irt
• Genetic Background: involves: C57BL/6 * C57BL/6J

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

reproductive system

female infertility ( J:154647 )

♀

immune system

decreased macrophage apoptosis ( J:154647 )

• macrophages exhibit less cholesterol-induced apoptosis and reduced loss of mitochondrial membrane potential compared with similarly treated wild-type cells

• tunicamycin-treated macrophages exhibit less apoptosis and no loss of mitochondrial membrane compared with similarly treated wild-type cells

• tunicamycin-treated CD68+ macrophages fail to exhibit apoptosis unlike similarly treated wild-type cells

homeostasis/metabolism

decreased susceptibility to injury ( J:154647 )

• tunicamycin-treated mice exhibit less renal tubular epithelium apoptosis and normal kidney function compared with similarly treated wild-type mice

cellular

decreased macrophage apoptosis ( J:154647 )

• macrophages exhibit less cholesterol-induced apoptosis and reduced loss of mitochondrial membrane potential compared with similarly treated wild-type cells

• tunicamycin-treated macrophages exhibit less apoptosis and no loss of mitochondrial membrane compared with similarly treated wild-type cells

• tunicamycin-treated CD68+ macrophages fail to exhibit apoptosis unlike similarly treated wild-type cells

hematopoietic system

decreased macrophage apoptosis ( J:154647 )

• macrophages exhibit less cholesterol-induced apoptosis and reduced loss of mitochondrial membrane potential compared with similarly treated wild-type cells

• tunicamycin-treated macrophages exhibit less apoptosis and no loss of mitochondrial membrane compared with similarly treated wild-type cells

• tunicamycin-treated CD68+ macrophages fail to exhibit apoptosis unlike similarly treated wild-type cells

Genotype
MGI:5927424

hm2

• Allelic Composition: Camk2g^tm1.1Irt/Camk2g^tm1.1Irt
• Genetic Background: involves: C57BL/6J

digestive/alimentary system

increased susceptibility to induced colitis ( J:243363 )

• mice treated with dextran sodium sulfate (DSS) to induce colitis exhibit more severe colitis-induced injury, showing shorter colon lengths, higher rectal bleeding rates, more inflammatory cell infiltration, ulceration and hyperplasia in the colon, decreased proliferation of colonic epithelial cells during the regeneration stage of colitis, have fewer proliferating crypts in inflamed colonic tissues, more apoptotic epithelial cells, and greater weight loss

• however, mice treated with DSS exhibit similar inflammatory cytokine and enzyme expression as wild-type mice

increased susceptibility to colitis induced morbidity/mortality ( J:243363 )

• 50% of mice challenged with DSS for 7 days die by 10 days after the start of DSS treatment

mortality/aging

increased susceptibility to colitis induced morbidity/mortality ( J:243363 )

• 50% of mice challenged with DSS for 7 days die by 10 days after the start of DSS treatment

neoplasm

decreased incidence of tumors by chemical induction ( J:243363 )

• mice injected with azoxymethane (AOM) followed by DSS administration develop fewer tumors and smaller tumors in the colon compared to wild-type controls

homeostasis/metabolism

decreased incidence of tumors by chemical induction ( J:243363 )

• mice injected with azoxymethane (AOM) followed by DSS administration develop fewer tumors and smaller tumors in the colon compared to wild-type controls

immune system

increased susceptibility to induced colitis ( J:243363 )

• mice treated with dextran sodium sulfate (DSS) to induce colitis exhibit more severe colitis-induced injury, showing shorter colon lengths, higher rectal bleeding rates, more inflammatory cell infiltration, ulceration and hyperplasia in the colon, decreased proliferation of colonic epithelial cells during the regeneration stage of colitis, have fewer proliferating crypts in inflamed colonic tissues, more apoptotic epithelial cells, and greater weight loss

• however, mice treated with DSS exhibit similar inflammatory cytokine and enzyme expression as wild-type mice

increased susceptibility to colitis induced morbidity/mortality ( J:243363 )

• 50% of mice challenged with DSS for 7 days die by 10 days after the start of DSS treatment