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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Fabp1-cre)1Jig
transgene insertion 1, Jeffrey I Gordon
MGI:2447212
Summary 20 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
ApcMin/Apc+
Dnmt3btm1Jae/Dnmt3btm1Jae
Tg(Fabp1-cre)1Jig/0
involves: 129 * C57BL/6 * C57BL/6J * FVB/N MGI:3625330
cn2
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N MGI:3776026
cn3
Apctm2.1Cip/Apc+
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
involves: 129P2/OlaHsd * 129S4/SvJae * FVB MGI:3776028
cn4
Ptentm2Mak/Ptentm2Mak
Tg(Fabp1-cre)1Jig/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N MGI:5004866
cn5
Apctm1Rsmi/Apc+
Ctnnb1tm1Wvv/Ctnnb1+
Tg(Fabp1-cre)1Jig/?
involves: 129P2/OlaHsd * C57BL/6J * FVB/N MGI:5430612
cn6
Apctm2.1Cip/Apc+
Tg(Fabp1-cre)1Jig/0
involves: 129P2/OlaHsd * FVB/N MGI:3776025
cn7
Apctm1Rsmi/Apc+
Tg(Fabp1-cre)1Jig/0
involves: 129P2/OlaHsd * FVB/N MGI:4456428
cn8
Hif1atm3Rsjo/Hif1atm3Rsjo
Tg(Fabp1-cre)1Jig/0
involves: 129S1/Sv * 129X1/SvJ * BALB/c * FVB/N MGI:4418471
cn9
Cdkn1atm1Tyj/Cdkn1atm1Tyj
Ptentm1Hwu/Ptentm1Hwu
Tg(Fabp1-cre)1Jig/0
involves: 129S2/SvPas * 129S4/SvJae * FVB/N MGI:4844100
cn10
Krastm1.1Khai/Kras+
Tg(Fabp1-cre)1Jig/0
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * FVB/N MGI:6505543
cn11
Apctm2Rak/Apc+
Krastm1.1Khai/Kras+
Tg(Fabp1-cre)1Jig/0
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * FVB/N * SJL MGI:6505557
cn12
Tg(Fabp1-cre)1Jig/0
Vhltm1Jae/Vhltm1Jae
involves: 129S4/SvJae * BALB/c * FVB/N MGI:4418472
cn13
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:6505545
cn14
Apctm2Rak/Apc+
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
involves: 129S4/SvJae * C57BL/6 * FVB/N * SJL MGI:6505558
cn15
Ptentm1Hwu/Ptentm1Hwu
Tg(Fabp1-cre)1Jig/0
involves: 129S4/SvJae * FVB/N MGI:4844083
cn16
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
involves: 129S4/SvJae * FVB/N MGI:3044567
cn17
Ccnftm1Sje/Ccnftm1.1Sje
Tg(Fabp1-cre)1Jig/0
involves: 129S7/SvEvBrd * C57BL/6 * FVB/N MGI:3041859
cn18
Atoh1tm2Hzo/Atoh1tm3Hzo
Tg(Fabp1-cre)1Jig/0
involves: 129S7/SvEvBrd * C57BL/6J * FVB/N * SJL MGI:3767181
cn19
Tnftm2.1Gkl/Tnftm2.1Gkl
Tg(Fabp1-cre)1Jig/0
involves: 129S/SvEv * FVB/N MGI:5558947
cn20
Nrastm1Tyj/Nras+
Tg(Fabp1-cre)1Jig/0
involves: C57BL/6 * FVB/N MGI:3776024


Genotype
MGI:3625330
cn1
Allelic
Composition
ApcMin/Apc+
Dnmt3btm1Jae/Dnmt3btm1Jae
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129 * C57BL/6 * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (12 available); any Apc mutation (158 available)
Dnmt3btm1Jae mutation (1 available); any Dnmt3b mutation (52 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• significant decrease in the formation of macroscopic colonic adenomas in ApcMin/+ mice
• no impact on microadenoma formation
• no noticeable effect on later stages of tumor growth




Genotype
MGI:3776026
cn2
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• large, prominent goblet cells develop in the colon
• mice develop widespread hyperplasia throughout the colonic epithelium
• colonic epithelium has a larger transit amplifying cell zone than wild-type; cells in the colonic epithelium have a higher mitotic index than in wild-type
• hyperplasia is typified by extreme lengthening of the crypts

endocrine/exocrine glands
• hyperplasia is typified by extreme lengthening of the crypts

cellular
• large, prominent goblet cells develop in the colon




Genotype
MGI:3776028
cn3
Allelic
Composition
Apctm2.1Cip/Apc+
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2.1Cip mutation (2 available); any Apc mutation (158 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• animals have greatly reduced life-span compared to mutants expressing wild-type Kras

neoplasm
• adenocarcinomas show uniform high-grade dysplasia, including large, fused glands with serrated borders, pseudostratified epithelium, loss of apical-basal polarity, and high nucleus to cytoplasm ratio
• mice have more tumors than mutants expressing wild-type Kras
• terminally differentiated cells are absent from tumors

digestive/alimentary system
• adenocarcinomas show uniform high-grade dysplasia, including large, fused glands with serrated borders, pseudostratified epithelium, loss of apical-basal polarity, and high nucleus to cytoplasm ratio
• mice have more tumors than mutants expressing wild-type Kras
• terminally differentiated cells are absent from tumors




Genotype
MGI:5004866
cn4
Allelic
Composition
Ptentm2Mak/Ptentm2Mak
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2Mak mutation (4 available); any Pten mutation (88 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mutants exhibit increased susceptibility to N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN)-induced bladder cancer, with 50% developing transitional cell carcinomas (TCC) and 25% developing carcinoma in situ (CIS) and dysplasia compared to 8% of wild-type mice developing TCC and 8% developing CIS and dysplasia at 16 weeks after BBN administration
• mutants develop spontaneous superficial papillary transitional cell carcinomas, with an incidence of 10% in 40-80 week old mutants

renal/urinary system
• mutants develop spontaneous superficial papillary transitional cell carcinomas, with an incidence of 10% in 40-80 week old mutants
• two mutants exhibit hydronephrosis due to presence of large cancers in the bladder or renal pelvis
• thickening of the urothelial layer by 8 weeks of age due to increases in cell number and cell size
• urothelial hyperplasia is due to increased proliferation of bladder epithelial cells
• absolute numbers of bladder epithelial cells are increased 1.6-fold over wild-type levels at 8 weeks of age and 2.6-fold at 48 weeks of age
• size of individual bladder epithelial cells is greater than control cells; increase in size is not due to polyploidy as both diploid and tetraploid cell fractions are increased

homeostasis/metabolism
• mutants exhibit increased susceptibility to N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN)-induced bladder cancer, with 50% developing transitional cell carcinomas (TCC) and 25% developing carcinoma in situ (CIS) and dysplasia compared to 8% of wild-type mice developing TCC and 8% developing CIS and dysplasia at 16 weeks after BBN administration

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
urinary bladder cancer DOID:11054 OMIM:109800
J:113388




Genotype
MGI:5430612
cn5
Allelic
Composition
Apctm1Rsmi/Apc+
Ctnnb1tm1Wvv/Ctnnb1+
Tg(Fabp1-cre)1Jig/?
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Rsmi mutation (1 available); any Apc mutation (158 available)
Ctnnb1tm1Wvv mutation (0 available); any Ctnnb1 mutation (49 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• significantly increased tumor load in the intestine of males but not females compared to heterozygous Apctm1Ecrm
• tumors in both the ilium and colon but smaller in size than in heterozygous Apctm1Ecrm

digestive/alimentary system
• significantly increased tumor load in the intestine of males but not females compared to heterozygous Apctm1Ecrm
• tumors in both the ilium and colon but smaller in size than in heterozygous Apctm1Ecrm




Genotype
MGI:3776025
cn6
Allelic
Composition
Apctm2.1Cip/Apc+
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129P2/OlaHsd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2.1Cip mutation (2 available); any Apc mutation (158 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• focal, pedunculated adencarcinomas develop in the colon; lesions are typically heterogeneous showing both low grade and malignant epithelium

digestive/alimentary system
• focal, pedunculated adencarcinomas develop in the colon; lesions are typically heterogeneous showing both low grade and malignant epithelium




Genotype
MGI:4456428
cn7
Allelic
Composition
Apctm1Rsmi/Apc+
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129P2/OlaHsd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Rsmi mutation (1 available); any Apc mutation (158 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice succumb to intestinal tumors later than Apctm1.1Ecrm

neoplasm
• mice develop intestinal tumors unlike wild-type mice with later premature death and fewer tumors than Apctm1.1Ecrm heterozygotes
• intestinal tumors develop predominantly in the large intestine that are larger than in Apctm1.1Ecrm heterozygotes
• large intestine tumors are pedunculated (polypoid) or sessile
• intestinal tumors develop predominantly in the large intestine
• intestinal tumors develop predominantly in the large intestine
• intestinal tumors develop predominantly in the large intestine

digestive/alimentary system
• mice develop intestinal tumors unlike wild-type mice with later premature death and fewer tumors than Apctm1.1Ecrm heterozygotes
• intestinal tumors develop predominantly in the large intestine that are larger than in Apctm1.1Ecrm heterozygotes
• large intestine tumors are pedunculated (polypoid) or sessile
• intestinal tumors develop predominantly in the large intestine
• intestinal tumors develop predominantly in the large intestine
• intestinal tumors develop predominantly in the large intestine

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
colorectal cancer DOID:9256 OMIM:114500
J:159883




Genotype
MGI:4418471
cn8
Allelic
Composition
Hif1atm3Rsjo/Hif1atm3Rsjo
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * BALB/c * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1atm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• hypoxia fails to induce an increase in colonic epithelial cell resistance unlike in similarly treated wild-type cells
• TNBS-treated mice exhibit more severe colitis, slower weight gain during recovery, decreased colon length, and increased mortality compared with similarly treated wild-type mice

immune system
• TNBS-treated mice exhibit more severe colitis, slower weight gain during recovery, decreased colon length, and increased mortality compared with similarly treated wild-type mice




Genotype
MGI:4844100
cn9
Allelic
Composition
Cdkn1atm1Tyj/Cdkn1atm1Tyj
Ptentm1Hwu/Ptentm1Hwu
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129S2/SvPas * 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn1atm1Tyj mutation (3 available); any Cdkn1a mutation (63 available)
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• bladder urothelium exhibits increased cell proliferation

neoplasm




Genotype
MGI:6505543
cn10
Allelic
Composition
Krastm1.1Khai/Kras+
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm1.1Khai mutation (1 available); any Kras mutation (84 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice show moderate colon epithelium crypt hyperplasia that is intermediate between wild-type mice and conditional Krastm4Tyj mice
• colons show an intermediate hyperproliferative phenotype compared to wild-type mice or conditional Krastm4Tyj mice
• Paneth cells are intact in colons

endocrine/exocrine glands
• mice show moderate colon epithelium crypt hyperplasia that is intermediate between wild-type mice and conditional Krastm4Tyj mice




Genotype
MGI:6505557
cn11
Allelic
Composition
Apctm2Rak/Apc+
Krastm1.1Khai/Kras+
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2Rak mutation (1 available); any Apc mutation (158 available)
Krastm1.1Khai mutation (1 available); any Kras mutation (84 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice develop colonic tumors, characterized as adenomas with low-grade dysplasia

mortality/aging
• mice show slightly longer survival than conditional mice carrying the Krastm4Tyj allele

digestive/alimentary system
• mice develop colonic tumors, characterized as adenomas with low-grade dysplasia

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
colorectal cancer DOID:9256 OMIM:114500
J:276349




Genotype
MGI:4418472
cn12
Allelic
Composition
Tg(Fabp1-cre)1Jig/0
Vhltm1Jae/Vhltm1Jae
Genetic
Background
involves: 129S4/SvJae * BALB/c * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Fabp1-cre)1Jig mutation (2 available)
Vhltm1Jae mutation (2 available); any Vhl mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice exposed to hypoxic conditions exhibit reduced impairment in intestinal barrier function compared with similarly treated wild-type mice
• TNBS-treated mice do not exhibit weight loss, as severe reduction in colon length, as much mortality, or an increase in intestinal permeability unlike similarly treated wild-type mice

immune system
• TNBS-treated mice do not exhibit weight loss, as severe reduction in colon length, as much mortality, or an increase in intestinal permeability unlike similarly treated wild-type mice




Genotype
MGI:6505545
cn13
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice show colon epithelium crypt hyperplasia that is greater than seen in conditional Krastm1.1Khai mice
• Paneth cells are absent in colons
• mice treated with trametinib show restoration of Paneth cell differentiation in colons
• colons show a greater hyperproliferative phenotype than in conditional Krastm1.1Khai mice

endocrine/exocrine glands
• mice show colon epithelium crypt hyperplasia that is greater than seen in conditional Krastm1.1Khai mice
• Paneth cells are absent in colons
• mice treated with trametinib show restoration of Paneth cell differentiation in colons




Genotype
MGI:6505558
cn14
Allelic
Composition
Apctm2Rak/Apc+
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2Rak mutation (1 available); any Apc mutation (158 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice develop colonic tumors, characterized as adenomas with low-grade dysplasia

mortality/aging
• mice show 100% lethality before 150 days of age

digestive/alimentary system
• mice develop colonic tumors, characterized as adenomas with low-grade dysplasia

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
colorectal cancer DOID:9256 OMIM:114500
J:276349




Genotype
MGI:4844083
cn15
Allelic
Composition
Ptentm1Hwu/Ptentm1Hwu
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system

mortality/aging
• only 45% of males survive to 13.5 months of age, compared to 75% of females surviving to this age

endocrine/exocrine glands
• hyperplasia in the anterior prostate is observed at 8 days of age
• within the first year of life, 97% of males develop tumors of the anterior prostate
• prostate tumors are carcinomas
• in males over one year of age, the tumor takes over the entire prostate and seminal vesicle

renal/urinary system
• hyperplasia in the urinary tract
• urothelial carcinoma of the kidney
• urothelial carcinoma of the bladder
• 22% of mutants exhibit bladder cancer by 13.5 months of age
• males exhibit hydronephrosis of the kidney
• epithelial hypertrophy and nuclear atypia are evident in bladders at birth
• 100% penetrance of hypertrophy and hyperplasia in the bladder by 6 weeks of age
• 1/3 of male deaths are due to inability to urinate due to urinary tract blockage
• females do not lose the ability to urinate

reproductive system
• hyperplasia in the anterior prostate is observed at 8 days of age
• within the first year of life, 97% of males develop tumors of the anterior prostate
• prostate tumors are carcinomas
• in males over one year of age, the tumor takes over the entire prostate and seminal vesicle

neoplasm
• within the first year of life, 97% of males develop tumors of the anterior prostate
• prostate tumors are carcinomas
• in males over one year of age, the tumor takes over the entire prostate and seminal vesicle
• metastasis of the bladder and urothelial carcinomas is observed
• urothelial carcinoma of the bladder, ureter, and kidney
• squamous cell carcinoma of the vagina and rectum
• carcinomas of the prostate, seminal vesicles and urethra
• urothelial carcinoma of the kidney
• 41% of females develop vaginal squamous cell carcinoma
• urothelial carcinoma of the bladder
• 22% of mutants exhibit bladder cancer by 13.5 months of age




Genotype
MGI:3044567
cn16
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• diffuse hyperplasia and dysplasia of the colonic crypts is seen by 4 weeks of age
• increased proliferation of the hyperplastic and dysplastic colonic epithelium is seen in mutants




Genotype
MGI:3041859
cn17
Allelic
Composition
Ccnftm1Sje/Ccnftm1.1Sje
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ccnftm1.1Sje mutation (0 available); any Ccnf mutation (51 available)
Ccnftm1Sje mutation (0 available); any Ccnf mutation (51 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• no developmental or physiological defects are detected in the distal small intestine, cecum, colon, or bladder




Genotype
MGI:3767181
cn18
Allelic
Composition
Atoh1tm2Hzo/Atoh1tm3Hzo
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6J * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atoh1tm2Hzo mutation (1 available); any Atoh1 mutation (37 available)
Atoh1tm3Hzo mutation (1 available); any Atoh1 mutation (37 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• unlike mice with complete recombination of the floxed allele in the entire intestinal epithelium, mice with a mosaic pattern of recombination show no increase in mortality up to at least 1 year of age

digestive/alimentary system
• the small intestine contains patches of abnormal crypts with a recombined allele mixed with areas of normal crypts with an unrecombined allele
• crypts with the recombined allele completely lack goblet, Paneth, and enteroendocrine cells instead containing only absorptive enterocytes
• a significant increase in BrdU+ cells and mitotic figures is seen in crypts with a recombined allele
• crypts with a recombined allele are smaller than neighboring crypts in which recombination did not occur
• the adaptive response following resection of the middle 50% of the small bowel is blunted with a smaller increase in crypt depth compared to control mice

endocrine/exocrine glands
• the small intestine contains patches of abnormal crypts with a recombined allele mixed with areas of normal crypts with an unrecombined allele
• crypts with the recombined allele completely lack goblet, Paneth, and enteroendocrine cells instead containing only absorptive enterocytes
• a significant increase in BrdU+ cells and mitotic figures is seen in crypts with a recombined allele
• crypts with a recombined allele are smaller than neighboring crypts in which recombination did not occur




Genotype
MGI:5558947
cn19
Allelic
Composition
Tnftm2.1Gkl/Tnftm2.1Gkl
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129S/SvEv * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Fabp1-cre)1Jig mutation (2 available)
Tnftm2.1Gkl mutation (1 available); any Tnf mutation (48 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• disruption of the mucosal architecture with prominent villous distortion characterized by widening and decreased number of villi
• increase in numbers of activated CD4+ cells within their intestinal mucosa
• prominent villous distortion characterized by widening and decreased number of villi
• low-grade inflammatory cell infiltration with both active and chronic components is seen in the colon
• chronic small intestinal inflammation
• mice exhibit severe inflammatory changes in the ilea, including dense infiltration of the lamina propria by acute (polymorphonuclear), but mainly chronic (lymphocytes, macrophages), inflammatory cells
• however, no inflammation is seen in other parts of the small intestine, including the jejunum , and mice do not develop inflammatory arthritis

immune system
• low-grade inflammatory cell infiltration with both active and chronic components is seen in the colon
• chronic small intestinal inflammation
• mice exhibit severe inflammatory changes in the ilea, including dense infiltration of the lamina propria by acute (polymorphonuclear), but mainly chronic (lymphocytes, macrophages), inflammatory cells
• however, no inflammation is seen in other parts of the small intestine, including the jejunum , and mice do not develop inflammatory arthritis

homeostasis/metabolism

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
inflammatory bowel disease DOID:0050589 OMIM:PS266600
J:204557




Genotype
MGI:3776024
cn20
Allelic
Composition
Nrastm1Tyj/Nras+
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nrastm1Tyj mutation (1 available); any Nras mutation (44 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• expression of mutant Nras appears to have no effect on the histology of the colonic epithelium





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
11/19/2024
MGI 6.24
The Jackson Laboratory