Phenotypes associated with this allele

• Allele Symbol: Mapkapk2^tm1.2Gkl
• Allele Name: targeted mutation 1.2, George Kollias
• Allele ID: MGI:6357679
• Summary: 2 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Mapkapk2^tm1.2Gkl/Mapkapk2^tm1.2Gkl	involves: BALB/cJ * C57BL/6	MGI:6357717
cx2	Apc^Min/Apc^+ Mapkapk2^tm1.2Gkl/Mapkapk2^tm1.2Gkl	involves: BALB/cJ * C57BL/6J	MGI:6357720

Genotype
MGI:6357717

hm1

• Allelic Composition: Mapkapk2^tm1.2Gkl/Mapkapk2^tm1.2Gkl
• Genetic Background: involves: BALB/cJ * C57BL/6

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

neoplasm

decreased incidence of tumors by chemical induction ( J:262876 )

• fewer smaller tumors induced by AOM/DSS

• however, development of induced colitis is normal

immune system

decreased circulating tumor necrosis factor level ( J:262876 )

• after LPS and D-galactosamine administration

decreased tumor necrosis factor secretion ( J:262876 )

• from thioglycollate-elicited peritoneal macrophages after LPS stimulation in vitro

homeostasis/metabolism

decreased circulating tumor necrosis factor level ( J:262876 )

• after LPS and D-galactosamine administration

decreased incidence of tumors by chemical induction ( J:262876 )

• fewer smaller tumors induced by AOM/DSS

• however, development of induced colitis is normal

Genotype
MGI:6357720

cx2

• Allelic Composition: Apc^Min/Apc⁺; Mapkapk2^tm1.2Gkl/Mapkapk2^tm1.2Gkl
• Genetic Background: involves: BALB/cJ * C57BL/6J

mortality/aging

increased tumor-free survival time ( J:262876 )

• mice exhibit increased survival compared with Apc^min heterozygotes

neoplasm

abnormal tumor vascularization ( J:262876 )

• reduced tumor angiogenesis to in Apc^min heterozygotes

• however, inflammation in tumors is the same as in Apc^min heterozygotes

increased intestinal adenoma incidence ( J:262876 )

• at 8 weeks, mice develop the same number of microadenomas as in Apc^min heterozygotes

• however, fewer microadenomas and adenomas at later time points

decreased tumor growth/size ( J:262876 )

• smaller tumors and microadenomas compared with Apc^min heterozygotes

decreased tumor incidence ( J:262876 )

• mice exhibit reduced number of tumor, adenomas and microadenomas compared with Apc^min heterozygotes

• mice fail to exhibit adenocarcinomas/carcinomas at 22 weeks unlike Apc^min heterozygotes

• due to reduced proliferation and increased apoptosis levels of tumor cells compared with Apc^min heterozygotes

• reduced proliferation compared with Apc^min heterozygotes

• chimera reconstitution experiments indicate that nonhematopoietic cells are responsible for tumor suppression

digestive/alimentary system

intestine polyps ( J:262876 )

• fewer than in Apc^min heterozygotes

increased intestinal adenoma incidence ( J:262876 )

• at 8 weeks, mice develop the same number of microadenomas as in Apc^min heterozygotes

• however, fewer microadenomas and adenomas at later time points

cardiovascular system

abnormal tumor vascularization ( J:262876 )

• reduced tumor angiogenesis to in Apc^min heterozygotes

• however, inflammation in tumors is the same as in Apc^min heterozygotes

hematopoietic system

hematopoietic system phenotype ( J:262876 )

N • mice exhibit normal spleen size unlike Apc^min heterozygotes

immune system

abnormal chemokine secretion ( J:262876 )

• decreased secretion of MIP2 and MMP9 from intestinal mesenchymal cells in culture stimulated with IL1beta, TNF or TGFbeta compared with cells from Apc^min heterozygotes

decreased interleukin-6 secretion ( J:262876 )

• from intestinal mesenchymal cells in culture stimulated with IL1beta, TNF or TGFbeta compared with cells from Apc^min heterozygotes