Phenotypes associated with this allele

• Allele Symbol: Rassf1^tm1.2Brd
• Allele Name: targeted mutation 1.2, Allan Bradley
• Allele ID: MGI:3604205
• Summary: 2 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Rassf1^tm1.2Brd/Rassf1^tm1.2Brd	involves: 129S7/SvEvBrd	MGI:4837483
hm2	Rassf1^tm1.2Brd/Rassf1^tm1.2Brd	involves: 129S7/SvEvBrd * C57BL/6	MGI:3606983

Genotype
MGI:4837483

hm1

• Allelic Composition: Rassf1^tm1.2Brd/Rassf1^tm1.2Brd
• Genetic Background: involves: 129S7/SvEvBrd

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

cardiovascular system

cardiac hypertrophy ( J:165327 )

• following pressure overload hypertrophy is increased compared to wild-type controls

cardiac fibrosis ( J:165327 )

• following pressure overload fibrosis is increased compared to wild-type controls

increased response of heart to induced stress ( J:165327 )

• following pressure overload hypertrophy and fibrosis are both increased and cardiomyocyte apoptosis is decreased compared to wild-type controls

• treatment with a TNF neutralizing antibody significantly attenuates the increase in hypertrophy and fibrosis and improves cardiac funtion following pressure overload

• in the absence of pressure overload, gross cardiac morphology is similar to controls

homeostasis/metabolism

increased response of heart to induced stress ( J:165327 )

• following pressure overload hypertrophy and fibrosis are both increased and cardiomyocyte apoptosis is decreased compared to wild-type controls

• treatment with a TNF neutralizing antibody significantly attenuates the increase in hypertrophy and fibrosis and improves cardiac funtion following pressure overload

• in the absence of pressure overload, gross cardiac morphology is similar to controls

growth/size/body

cardiac hypertrophy ( J:165327 )

• following pressure overload hypertrophy is increased compared to wild-type controls

Genotype
MGI:3606983

hm2

• Allelic Composition: Rassf1^tm1.2Brd/Rassf1^tm1.2Brd
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6

digestive/alimentary system

increased intestinal adenocarcinoma incidence ( J:101369 )

• an increased incidence of gastrointestinal adenomas and adenocarcinomas is also seen

mortality/aging

increased mortality induced by ionizing radiation ( J:101369 )

• after irradiation with 3.5 Gy at 4 weeks of age increased mortality (69% mortality) is seen compared to similarly treated wild-type mice (52% mortality)

premature death ( J:101369 )

• during the study 50% of homozygous mice died compared to 30% of wild-type mice

neoplasm

increased intestinal adenocarcinoma incidence ( J:101369 )

• an increased incidence of gastrointestinal adenomas and adenocarcinomas is also seen

increased adenoma incidence ( J:101369 )

• an increased incidence of gastrointestinal adenomas and adenocarcinomas is also seen

increased lymphoma incidence ( J:101369 )

• the most common form of cancer in these mice is lymphoma

increased incidence of tumors by ionizing radiation induction ( J:101369 )

• after irradiation with 3.5 Gy at 4 weeks of age an increased incidence of tumors is seen

cellular

abnormal cell physiology ( J:101369 )

• MEFs are more sensitive to microtubule depolymerization by nocodazole but display normal growth curves and cell cycle, do not display any evidence of genomic instability, and are not more sensitive to DNA damage or microtubule-binding agents

immune system

immune system phenotype ( J:101369 )

N • spleen and thymus weight, thymocyte numbers, and T cell population proportions are normal

homeostasis/metabolism

increased mortality induced by ionizing radiation ( J:101369 )

• after irradiation with 3.5 Gy at 4 weeks of age increased mortality (69% mortality) is seen compared to similarly treated wild-type mice (52% mortality)