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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Trp73tm2Mak
targeted mutation 2, Tak Mak
MGI:4442798
Summary 3 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Trp73tm2Mak/Trp73tm2Mak either: B6.129P2-Trp73tm2Mak or (involves: 129P2/OlaHsd * C57BL/6J) MGI:4442799
cx2
Trp53tm1Brd/Trp53tm1Brd
Trp73tm2Mak/Trp73tm2Mak
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J MGI:4442800
cx3
Atmtm1Pmc/Atmtm1Pmc
Trp73tm2Mak/Trp73tm2Mak
involves: 129P2/OlaHsd * C57BL/6J MGI:4442801


Genotype
MGI:4442799
hm1
Allelic
Composition
Trp73tm2Mak/Trp73tm2Mak
Genetic
Background
either: B6.129P2-Trp73tm2Mak or (involves: 129P2/OlaHsd * C57BL/6J)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp73tm2Mak mutation (1 available); any Trp73 mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• the gender ratio was slightly but significantly skewed at birth with fewer females being born than males

nervous system
• neuronal density is significantly reduced in the motor cortex at 10 and 26-27 months of age
• by 26-27 mo of age, motor cortex thickness is reduced significantly
• neuronal density is significantly reduced in the motor cortex at 10 and 26-27 months of age
• signs of mild neurodegeneration are seen such as an increase in the number of condensed cells at 10 months of age

hematopoietic system
• increased apoptosis in response to DNA damaging agents (cisplatin, doxorubicin, etoposide and gamma-irradiation)

immune system
• increased apoptosis in response to DNA damaging agents (cisplatin, doxorubicin, etoposide and gamma-irradiation)

homeostasis/metabolism
• both MEFs and thymocytes show increased sensitivity to DNA damaging agents including, cisplatin, doxorubicin and etoposide

cellular
• increased apoptosis in response to DNA damaging agents (cisplatin, doxorubicin, etoposide and gamma-irradiation)
• both MEFs and thymocytes show increased sensitivity to DNA damaging agents including, cisplatin, doxorubicin and etoposide
• however, no difference in the apoptotic response to UV treatment, TNFalpha treatment, or IL-2 withdrawal is detected
• both MEFs and thymocytes show increased sensitivity to gamma irradiation induced apoptosis

endocrine/exocrine glands
• increased apoptosis in response to DNA damaging agents (cisplatin, doxorubicin, etoposide and gamma-irradiation)




Genotype
MGI:4442800
cx2
Allelic
Composition
Trp53tm1Brd/Trp53tm1Brd
Trp73tm2Mak/Trp73tm2Mak
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Brd mutation (7 available); any Trp53 mutation (152 available)
Trp73tm2Mak mutation (1 available); any Trp73 mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• the increased apoptosis in response to DNA damaging agents is reversed compared to mice homozygous for Trp73 tm2Mak alone, returning it to wild-type levels

immune system
• the increased apoptosis in response to DNA damaging agents is reversed compared to mice homozygous for Trp73 tm2Mak alone, returning it to wild-type levels

cellular
• the increased apoptosis in response to DNA damaging agents is reversed compared to mice homozygous for Trp73 tm2Mak alone, returning it to wild-type levels
• the increased apoptosis in response to gamma-irradiation is reversed compared to mice homozygous for Trp73 tm2Mak alone, returning it to wild-type levels

endocrine/exocrine glands
• the increased apoptosis in response to DNA damaging agents is reversed compared to mice homozygous for Trp73 tm2Mak alone, returning it to wild-type levels




Genotype
MGI:4442801
cx3
Allelic
Composition
Atmtm1Pmc/Atmtm1Pmc
Trp73tm2Mak/Trp73tm2Mak
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atmtm1Pmc mutation (0 available); any Atm mutation (32 available)
Trp73tm2Mak mutation (1 available); any Trp73 mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• the increased apoptosis in response to DNA damaging agents is reversed compared to Trp73 tm2Mak single mutants, with cells showing reisistance to apoptosis similar to that in Atmtm1Pmc single mutants

immune system
• the increased apoptosis in response to DNA damaging agents is reversed compared to Trp73 tm2Mak single mutants, with cells showing reisistance to apoptosis similar to that in Atmtm1Pmc single mutants

cellular
• the increased apoptosis in response to DNA damaging agents is reversed compared to Trp73 tm2Mak single mutants, with cells showing reisistance to apoptosis similar to that in Atmtm1Pmc single mutants
• the increased thymocyte apoptosis in response to gamma-irradiation is reversed compared to mice homozygous for Trp73 tm2Mak single mutants, with cells showing reisistance to apoptosis similar to that in Atmtm1Pmc single mutants

endocrine/exocrine glands
• the increased apoptosis in response to DNA damaging agents is reversed compared to Trp73 tm2Mak single mutants, with cells showing reisistance to apoptosis similar to that in Atmtm1Pmc single mutants





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB), Gene Ontology (GO)
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last database update
01/14/2020
MGI 6.14
The Jackson Laboratory