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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Gt(ROSA)26Sortm1(cre/ERT)Brn
targeted mutation 1, Anton Berns
MGI:2445311
Summary 13 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sortm1(cre/ERT)Brn
Pou5f1tm1Jnic/Pou5f1tm1Jnic
involves: 129P2/OlaHsd MGI:5610125
cn2
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
Trp53bp2tm2Xlu/Trp53bp2tm2Xlu
involves: 129P2/OlaHsd MGI:4819169
cn3
Tbx4tm1.2Pa/Tbx4tm1.2Pa
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * FVB/N MGI:3811615
cn4
Nrbp1tm1.1Dja/Nrbp1tm1.2Dja
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
involves: 129P2/OlaHsd * 129S4/SvJaeSor * 129S7/SvEvBrd * C57BL/6J MGI:5427573
cn5
Nrbp1tm1.1Dja/Nrbp1tm1.1Dja
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6J MGI:5427574
cn6
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
Lin9tm1.1Sgau/Lin9tm1.1Sgau
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * SJL MGI:4819582
cn7
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
Lin9tm1.1Sgau/Lin9+
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * SJL MGI:4819583
cn8
Atg3tm1.1Ywh/Atg3tm1.1Ywh
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
involves: 129P2/OlaHsd * 129S/SvEv * 129S4/SvJaeSor * C57BL/6 MGI:5009307
cn9
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
Ppp1r13ltm1Xlu/Ppp1r13ltm1Xlu
involves: 129P2/OlaHsd * 129S/SvEv * C57BL/6J MGI:5295149
cn10
Cdc25atm1Hpw/Cdc25atm1.1Hpw
Cdc25btm1Pjd/Cdc25btm1Pjd
Cdc25ctm1Hpw/Cdc25ctm1Hpw
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 MGI:3845392
cn11
Cdc25atm1Hpw/Cdc25atm1.1Hpw
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 MGI:3845383
cn12
Fbxo43tm1.1Kald/Fbxo43tm1.2Kald
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
involves: 129P2/OlaHsd * C57BL/6 * FVB/N * SJL MGI:6201521
cn13
Cdk1tm3Kald/Cdk1+
Fbxo43tm1.2Kald/Fbxo43tm1.2Kald
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
involves: 129P2/OlaHsd * C57BL/6 * FVB/N * SJL MGI:6201527


Genotype
MGI:5610125
cn1
Allelic
Composition
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sortm1(cre/ERT)Brn
Pou5f1tm1Jnic/Pou5f1tm1Jnic
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Brn mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Pou5f1tm1Jnic mutation (0 available); any Pou5f1 mutation (82 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
embryo
• embryos isolated at the 8 cell stage then treated with 4-hydroxytamoxifen (4-OHT) for 24 hours then examined 24 hours later show impaired formation of the primitive endoderm
• impaired lineage segregation of the ICM in 4-OHT treated cultured embryos
• after 5 days in culture 4-OHT treated embryos produce sheets of trophoblast giant cells with no discernible ICM or primitive endoderm derivatives




Genotype
MGI:4819169
cn2
Allelic
Composition
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
Trp53bp2tm2Xlu/Trp53bp2tm2Xlu
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Brn mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Trp53bp2tm2Xlu mutation (0 available); any Trp53bp2 mutation (53 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• in culture primary kidney epithelial cells show a delay in the formation of mature cell junctions




Genotype
MGI:3811615
cn3
Allelic
Composition
Tbx4tm1.2Pa/Tbx4tm1.2Pa
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Brn mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Tbx4tm1.2Pa mutation (1 available); any Tbx4 mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• following tamoxifen treatment at E6.5, all mice die at E10.5 due to failure of chorioallantoic fusion
• following tamoxifen treatment at E7.5, 50% of mice die at E10.5 due to failure of chorioallantoic fusion

limbs/digits/tail
N
• despite defects in hindlimb formation following treatment with tamoxifen at E9.5 and E10.5, mice exhibit normal hindlimb identity and forelimb development
• mice treated with tamoxifen at E11.5 exhibit normal hindlimb morphology
• following tamoxifen treatment at E7.5, limb buds form but are degenerating by E11.5 with hindlimb limited outgrowth
• following tamoxifen treatment at E9.5, the autopod of the hindlimb is thin
• following tamoxifen treatment at E9.5, the space between expression domains of Tbx2 and Tbx3 expression are narrower than in wild type mice and the hindlimb autopod contains fewer cells than in wild-type mice
• however, there is no reduction in cell proliferation rates in the hindlimb autopods of tamoxifen treated mice
• following tamoxifen treatment at E9.5 or E10.5, mice exhibit abnormal anterior digits of the hindlimb
• following tamoxifen treatment at E10.5, some mice exhibit thin hindlimb digits I and II
• following tamoxifen treatment at E9.5, 33% of mice exhibit fusion of the anterior hindlimb digit; some with parital fusions of digits I and II and others with 4 digits indicating the loss of digit II or fusion of digits I and II
• following tamoxifen treatment at E10.5, 42% of mice exhibit fusion of the anterior hindlimb digits
• following tamoxifen treatment at E9.5, 67% of mice exhibit four symmetrical hindlimb digits
• following tamoxifen treatment at E9.5, digits I and II are partially fused in some mice while others have 4 digits indicating the loss of digit II or fusion of digits I and II
• following tamoxifen treatment at E9.5 or E10.5, mice exhibit aplastic or severely hypoplastic femurs that do not articulate with the pelvis
• following tamoxifen treatment at E9.5 or E10.5, mice exhibit aplastic or severely hypoplastic femurs that do not articulate with the pelvis
• following tamoxifen treatment at E9.5 or E10.5, mice exhibit hypoplastic fibulas
• following tamoxifen treatment at E9.5 and E10.5, the hindlimb is shorter than in wild type mice at E14.5
• following tamoxifen treatment at E10.5, some mice exhibit a metatarsal of the first digit that originates near the middle of the metatarsal of digit two instead of near the tarsal bone

embryo
• following tamoxifen treatment at E7.5, limb buds form but are degenerating by E11.5 with hindlimb limited outgrowth
• following tamoxifen treatment at E6.5, mice die at E10.5 due to failure of chorioallantoic fusion
• following tamoxifen treatment at E7.5, 50% of mice die at E10.5 due to failure of chorioallantoic fusion

skeleton
• following tamoxifen treatment at E9.5, 33% of mice exhibit fusion of the anterior hindlimb digit; some with parital fusions of digits I and II and others with 4 digits indicating the loss of digit II or fusion of digits I and II
• following tamoxifen treatment at E10.5, 42% of mice exhibit fusion of the anterior hindlimb digits
• following tamoxifen treatment at E9.5 or E10.5, mice exhibit aplastic or severely hypoplastic femurs that do not articulate with the pelvis
• following tamoxifen treatment at E9.5 or E10.5, mice exhibit aplastic or severely hypoplastic femurs that do not articulate with the pelvis
• following tamoxifen treatment at E9.5 or E10.5, mice exhibit hypoplastic fibulas
• following tamoxifen treatment at E10.5, some mice exhibit a metatarsal of the first digit that originates near the middle of the metatarsal of digit two instead of near the tarsal bone
• following tamoxifen treatment at E9.5 or E10.5, mice exhibit abnormal pelvic connections and hypoplastic pelvises




Genotype
MGI:5427573
cn4
Allelic
Composition
Nrbp1tm1.1Dja/Nrbp1tm1.2Dja
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJaeSor * 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Brn mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Nrbp1tm1.1Dja mutation (0 available); any Nrbp1 mutation (52 available)
Nrbp1tm1.2Dja mutation (0 available); any Nrbp1 mutation (52 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• in tamoxifen-treated mice

mortality/aging
• moribund as early as 3 days post tamoxifen treatment
• 75% of mice die 9 days after tamoxifen treatment
• mice treated with a low dose of tamoxifen exhibit increased death associated with tumorigenesis

digestive/alimentary system
• tamoxifen-treated mice exhibit increased cell proliferation in the intestinal epithelium compared with control mice
• loss of architecture in tamoxifen-treated mice with reduction in numbers of differentiated cells, cells showing dysplastic nuclear atypia, widespread crypt elongation, increased crypt fission and reduction in villous length
• in tamoxifen-treated mice
• tamoxifen-treated mice exhibit a decrease of Alcian Blue positive goblet cells compared with control mice
• reduced numbers in tamoxifen-treated mice
• elongated in tamoxifen-treated mice
• altered distribution in tamoxifen-treated mice
• in tamoxifen-treated mice
• in tamoxifen-treated mice
• in 6 of 16 tamoxifen-treated mice, 2 of which are adenomas with high-grade dysplasia and 2 are invasive adenocarcinoma
• 5 of 6 tumors are located in the caecum

neoplasm
• tamoxifen-treated mice exhibit increased incidence of tumorigenesis, including lymphomas/leukemias and solid tumors (angiosarcoma, gastrointestinal adenoma, gastrointestinal adenocarcinoma and lung carcinoma)
• in 6 of 16 tamoxifen-treated mice, 2 of which are adenomas with high-grade dysplasia and 2 are invasive adenocarcinoma
• 5 of 6 tumors are located in the caecum
• in tamoxifen-treated mice
• in tamoxifen-treated mice
• in tamoxifen-treated mice

liver/biliary system
• tamoxifen-treated mice exhibit zone 3 hydropic changes indicative of malnutrition unlike control mice

homeostasis/metabolism
• in tamoxifen-treated mice

cellular
• tamoxifen-treated mice exhibit a decrease of Alcian Blue positive goblet cells compared with control mice
• tamoxifen-treated mice exhibit increased cell proliferation in the intestinal epithelium compared with control mice

endocrine/exocrine glands
• elongated in tamoxifen-treated mice
• altered distribution in tamoxifen-treated mice




Genotype
MGI:5427574
cn5
Allelic
Composition
Nrbp1tm1.1Dja/Nrbp1tm1.1Dja
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Brn mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Nrbp1tm1.1Dja mutation (0 available); any Nrbp1 mutation (52 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• moribund as early as 3 days post tamoxifen treatment
• 75% of mice die 9 days after tamoxifen treatment
• mice treated with a low dose of tamoxifen exhibit increased death associated with tumorigenesis

respiratory system
• in tamoxifen-treated mice

digestive/alimentary system
• tamoxifen-treated mice exhibit increased cell proliferation in the intestinal epithelium compared with control mice
• loss of architecture in tamoxifen-treated mice with reduction in numbers of differentiated cells, cells showing dysplastic nuclear atypia, widespread crypt elongation, increased crypt fission and reduction in villous length
• in tamoxifen-treated mice
• tamoxifen-treated mice exhibit a decrease of Alcian Blue positive goblet cells compared with control mice
• reduced numbers in tamoxifen-treated mice
• elongated in tamoxifen-treated mice
• altered distribution in tamoxifen-treated mice
• in tamoxifen-treated mice
• in tamoxifen-treated mice
• in 6 of 16 tamoxifen-treated mice, 2 of which are adenomas with high-grade dysplasia and 2 are invasive adenocarcinoma
• 5 of 6 tumors are located in the caecum

neoplasm
• tamoxifen-treated mice exhibit increased incidence of tumorigenesis, including lymphomas/leukemias and solid tumors (angiosarcoma, gastrointestinal adenoma, gastrointestinal adenocarcinoma and lung carcinoma)
• in 6 of 16 tamoxifen-treated mice, 2 of which are adenomas with high-grade dysplasia and 2 are invasive adenocarcinoma
• 5 of 6 tumors are located in the caecum
• in tamoxifen-treated mice
• in tamoxifen-treated mice
• in tamoxifen-treated mice

liver/biliary system
• tamoxifen-treated mice exhibit zone 3 hydropic changes indicative of malnutrition unlike control mice

homeostasis/metabolism
• in tamoxifen-treated mice

cellular
• tamoxifen-treated mice exhibit a decrease of Alcian Blue positive goblet cells compared with control mice
• tamoxifen-treated mice exhibit increased cell proliferation in the intestinal epithelium compared with control mice

endocrine/exocrine glands
• elongated in tamoxifen-treated mice
• altered distribution in tamoxifen-treated mice




Genotype
MGI:4819582
cn6
Allelic
Composition
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
Lin9tm1.1Sgau/Lin9tm1.1Sgau
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Brn mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Lin9tm1.1Sgau mutation (0 available); any Lin9 mutation (49 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• adult mice die 7 days after tamoxifen treatment

digestive/alimentary system
• tamoxifen-treated mice exhibit reduced cell proliferation with abnormal nuclei and mitotic increased nuclear area compared with wild-type mice
• tamoxifen-treated mice exhibit atrophy of the small intestine compared with wild-type mice
• 6 days after tamoxifen treatment, mice exhibit a greater than 80% loss of villus epithelium compared with wild-type mice however, no increase in apoptosis is observed

cellular
• tamoxifen-treated mouse embryonic fibroblasts exhibit supernumerary centrosomes compared with similarly treated wild-type cells
• tamoxifen-treated mouse embryonic fibroblasts stimulated with serum exhibit abnormal nuclei including binuclear, multi-lobed, and donut-shaped nuclei compared to similarly treated wild-type cells
• tamoxifen-treated mouse embryonic fibroblasts exhibit a delayed entry into mitosis (G2 delay) compared with similarly treated wild-type mice
• tamoxifen-treated mouse embryonic fibroblasts exhibit mitotic errors including chromatin bridges, failed nuclear segregation, cytokinesis failure, chaotic multipolar spindles, and supernumerary centrosomes compared with similarly treated wild-type cells
• following tamoxifen treatment, mouse embryonic fibroblasts exhibit severely impaired proliferation compared with similarly treated wild-type cells
• tamoxifen-treated mice exhibit reduced cell proliferation with abnormal nuclei and mitotic increased nuclear area compared with wild-type mice




Genotype
MGI:4819583
cn7
Allelic
Composition
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
Lin9tm1.1Sgau/Lin9+
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Brn mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Lin9tm1.1Sgau mutation (0 available); any Lin9 mutation (49 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• mouse embryonic fibroblasts treated with tamoxifen and nocodazole exhibit reduced cell cycle arrest compared with similarly treated wild-type mice




Genotype
MGI:5009307
cn8
Allelic
Composition
Atg3tm1.1Ywh/Atg3tm1.1Ywh
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
Genetic
Background
involves: 129P2/OlaHsd * 129S/SvEv * 129S4/SvJaeSor * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atg3tm1.1Ywh mutation (0 available); any Atg3 mutation (19 available)
Gt(ROSA)26Sortm1(cre/ERT)Brn mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• following tamoxifen stimulation
• however, apoptosis is rescued by IL7 treatment
• T lymphocytes exhibit increased mitochondria and endoplasmic reticulum content compared with wild-type cells

hematopoietic system
• following tamoxifen stimulation
• however, apoptosis is rescued by IL7 treatment
• T lymphocytes exhibit increased mitochondria and endoplasmic reticulum content compared with wild-type cells

cellular
• following tamoxifen stimulation
• however, apoptosis is rescued by IL7 treatment




Genotype
MGI:5295149
cn9
Allelic
Composition
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
Ppp1r13ltm1Xlu/Ppp1r13ltm1Xlu
Genetic
Background
involves: 129P2/OlaHsd * 129S/SvEv * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Brn mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Ppp1r13ltm1Xlu mutation (0 available); any Ppp1r13l mutation (39 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• tamoxifen-treated mouse embryonic fibroblasts exhibit a dramatic reduction of S phase entry compared with control mice
• tamoxifen-treated primary keratinocyte cultures exhibit increased expression of differentiation markers compared with control cells
• tamoxifen-treated mouse embryonic fibroblasts exhibit decreased proliferation and a 2- to 6-fold increase in slow cycling cells in passage 4 and 5 compared with control mice
• in tamoxifen-treated mouse embryonic fibroblasts

integument
• tamoxifen-treated primary keratinocyte cultures exhibit increased expression of differentiation markers compared with control cells




Genotype
MGI:3845392
cn10
Allelic
Composition
Cdc25atm1Hpw/Cdc25atm1.1Hpw
Cdc25btm1Pjd/Cdc25btm1Pjd
Cdc25ctm1Hpw/Cdc25ctm1Hpw
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
Genetic
Background
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdc25atm1.1Hpw mutation (1 available); any Cdc25a mutation (34 available)
Cdc25atm1Hpw mutation (1 available); any Cdc25a mutation (34 available)
Cdc25btm1Pjd mutation (0 available); any Cdc25b mutation (30 available)
Cdc25ctm1Hpw mutation (1 available); any Cdc25c mutation (23 available)
Gt(ROSA)26Sortm1(cre/ERT)Brn mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Shortened villi in the small intestine of Cdc25atm1Hpw/Cdc25atm1.1Hpw Cdc25btm1Pjd/Cdc25btm1Pjd Cdc25ctm1Hpw/Cdc25ctm1Hpw Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+ (TKO) mice

mortality/aging
• adult mice die within 1 week of initial 4-hydroxytamoxifen (OHT) injection

growth/size/body
• adult mice exhibit significant weight loss (20%) within 1 week of initial tamoxifen injection

digestive/alimentary system
• profound cell atrophy in the crypts is observed in OHT-treated mice; crypts are >40% smaller in mutants than Cdc25a-single knockout controls, with the crypt width being decreased more significantly than the depth
• a 70% loss of epithelial cells per crypt is detected, but no difference in mature Paneth cells is observed
• decreased proliferation of epithelial cells is observed, with no significant increase in apoptotic cell numbers; this results in premature differentiation of cell progenitors below Paneth cell compartments in crypts
• crypts have increased numbers of cells exhibiting early differentiation with no crypt base columnar (CBC) cells
• villi are lined with shorter, less-dense enterocytes in proximal regions; complete loss of distal villi is observed in some areas
• significant loss of villus height in proximal and distal regions is observed in mutants after OHT treatment
• 6 days following the final of 3 consecutive injections of tamoxifen, length of small intestine is shortened by 40% compared to controls

endocrine/exocrine glands
• profound cell atrophy in the crypts is observed in OHT-treated mice; crypts are >40% smaller in mutants than Cdc25a-single knockout controls, with the crypt width being decreased more significantly than the depth
• a 70% loss of epithelial cells per crypt is detected, but no difference in mature Paneth cells is observed
• decreased proliferation of epithelial cells is observed, with no significant increase in apoptotic cell numbers; this results in premature differentiation of cell progenitors below Paneth cell compartments in crypts
• crypts have increased numbers of cells exhibiting early differentiation with no crypt base columnar (CBC) cells




Genotype
MGI:3845383
cn11
Allelic
Composition
Cdc25atm1Hpw/Cdc25atm1.1Hpw
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
Genetic
Background
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdc25atm1.1Hpw mutation (1 available); any Cdc25a mutation (34 available)
Cdc25atm1Hpw mutation (1 available); any Cdc25a mutation (34 available)
Gt(ROSA)26Sortm1(cre/ERT)Brn mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• no difference in villi height is after 4-hydroxytamoxifen treatment observed after in contrast to triple knockout mice




Genotype
MGI:6201521
cn12
Allelic
Composition
Fbxo43tm1.1Kald/Fbxo43tm1.2Kald
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fbxo43tm1.1Kald mutation (0 available); any Fbxo43 mutation (29 available)
Fbxo43tm1.2Kald mutation (0 available); any Fbxo43 mutation (29 available)
Gt(ROSA)26Sortm1(cre/ERT)Brn mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• at stage XII (pachytene/diplotene) in tamoxifen-treated mice
• in tamoxifen-treated mice

cellular
• at stage XII (pachytene/diplotene) in tamoxifen-treated mice




Genotype
MGI:6201527
cn13
Allelic
Composition
Cdk1tm3Kald/Cdk1+
Fbxo43tm1.2Kald/Fbxo43tm1.2Kald
Gt(ROSA)26Sortm1(cre/ERT)Brn/Gt(ROSA)26Sor+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdk1tm3Kald mutation (0 available); any Cdk1 mutation (21 available)
Fbxo43tm1.2Kald mutation (0 available); any Fbxo43 mutation (29 available)
Gt(ROSA)26Sortm1(cre/ERT)Brn mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• within 4 to 5 days after treatment with tamoxifen at around age P21

reproductive system
• after treatment with tamoxifen at around age P21
• early in diplotene with some progression into metaphase
• after treatment with tamoxifen at around age P21

cellular
• after treatment with tamoxifen at around age P21
• early in diplotene with some progression into metaphase
• after treatment with tamoxifen at around age P21





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last database update
11/19/2024
MGI 6.24
The Jackson Laboratory