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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Gkn2tm1.1(KOMP)Vlcg
targeted mutation 1.1, Velocigene
MGI:5548517
Summary 3 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Gkn2tm1.1(KOMP)Vlcg/Gkn2tm1.1(KOMP)Vlcg C57BL/6N-Gkn2tm1.1(KOMP)Vlcg/Ucd MGI:5797561
hm2
Gkn2tm1.1(KOMP)Vlcg/Gkn2tm1.1(KOMP)Vlcg involves: C57BL/6NTac MGI:5898088
cx3
Gkn2tm1.1(KOMP)Vlcg/Gkn2tm1.1(KOMP)Vlcg
Il6sttm1Ern/Il6sttm1Ern
involves: 129S1/Sv * C57BL/6NTac MGI:5898089


Genotype
MGI:5797561
hm1
Allelic
Composition
Gkn2tm1.1(KOMP)Vlcg/Gkn2tm1.1(KOMP)Vlcg
Genetic
Background
C57BL/6N-Gkn2tm1.1(KOMP)Vlcg/Ucd
Cell Lines 14915A-B3
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gkn2tm1.1(KOMP)Vlcg mutation (1 available); any Gkn2 mutation (22 available)
Data Sources
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue

cardiovascular system
IMPC - UCD

growth/size/body
IMPC - UCD

hematopoietic system

homeostasis/metabolism

limbs/digits/tail
IMPC - UCD

nervous system




Genotype
MGI:5898088
hm2
Allelic
Composition
Gkn2tm1.1(KOMP)Vlcg/Gkn2tm1.1(KOMP)Vlcg
Genetic
Background
involves: C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gkn2tm1.1(KOMP)Vlcg mutation (1 available); any Gkn2 mutation (22 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• abnormalities of the corpus mucosa including focal hypertrophic lesions that are detectable at 6 weeks of age and persist at 12 and 30 weeks of age
• increased incidence of mucus neck cell hyperplasia in the corpus mucosa at 6 and 12 weeks of age
• surface mucus cells show shift from neutral to acidic indicating metaplasia at 6 and 12 weeks of age
• hyperplasia and metaplasia remain elevated at 30 weeks of age
• however, the antral mucosa has normal morphology
• increased incidence in the corpus mucosa at 6 and 12 weeks of age
• increased proliferation of gastric corpus mucosal epithelial cell proliferation at 6 and 12 but not 30 weeks of age
• increased incidence in the corpus mucosa at 6 and 12 weeks of age
• increased severity of H. pylori-induced atrophic gastritis and pervasive mucus metaplasia in the corpus compared to wild-type controls that show mild inflammation with infrequent atrophy and metaplasia
• however, antral inflammation scores after H. pylori infection are similar to wild-type controls

immune system
• increased incidence in the corpus mucosa at 6 and 12 weeks of age
• increased severity of H. pylori-induced atrophic gastritis and pervasive mucus metaplasia in the corpus compared to wild-type controls that show mild inflammation with infrequent atrophy and metaplasia
• however, antral inflammation scores after H. pylori infection are similar to wild-type controls
• antibody and cytokine responses indicate an increased Th1 immune response following H. pylori infection
• increased CXCL1 and CCL4 levels in corpus but not antral gastric tissues
• increased IL16, IL10, and IL1A levels in corpus but not antral gastric tissues
• increased TNF level in corpus but not antral gastric tissues
• increased mucosal innate immunity and impaired myeloid-derived suppressor cell responses in mice infected with H. pylori
• 7 days after H. pylori infection colonization levels are reduced in the gastric mucosa
• increased severity of H. pylori-induced atrophic gastritis and pervasive mucus metaplasia in the corpus compared to wild-type controls that show mild inflammation with infrequent atrophy and metaplasia
• however, antral inflammation scores after H. pylori infection are similar to wild-type controls

hematopoietic system
• decrease in the number of monocytic myeloid-derived suppressor cells in the stomach both before and during H. pylori infection
• antibody and cytokine responses indicate an increased Th1 immune response following H. pylori infection

endocrine/exocrine glands
• increased incidence in the corpus mucosa at 6 and 12 weeks of age

cellular
• impaired basal gastric epithelial differentiation

homeostasis/metabolism
• increased CXCL1 and CCL4 levels in corpus but not antral gastric tissues
• increased IL16, IL10, and IL1A levels in corpus but not antral gastric tissues
• increased TNF level in corpus but not antral gastric tissues




Genotype
MGI:5898089
cx3
Allelic
Composition
Gkn2tm1.1(KOMP)Vlcg/Gkn2tm1.1(KOMP)Vlcg
Il6sttm1Ern/Il6sttm1Ern
Genetic
Background
involves: 129S1/Sv * C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gkn2tm1.1(KOMP)Vlcg mutation (1 available); any Gkn2 mutation (22 available)
Il6sttm1Ern mutation (13 available); any Il6st mutation (80 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• corpus tumors display poorly differentiated and hyperplastic epithelium histologically
• in the corpus mucosa as a result of tumor formation
• however, antral mucosa thickness is similar to Il6st single mutants
• unlike Il6st single mutants which develop primarily antral tumors, double mutants show extensive focal tumorigenesis of the corpus and squamous epithelium overlying the limiting ridge of the corpus/forestomach junction at 12 weeks of age
• increase in both the number of corpus tumor foci and macroscopic corpus tumor area
• however, antral tumor load is similar to Il6st single mutants

neoplasm
• unlike Il6st single mutants which develop primarily antral tumors, double mutants show extensive focal tumorigenesis of the corpus and squamous epithelium overlying the limiting ridge of the corpus/forestomach junction at 12 weeks of age
• increase in both the number of corpus tumor foci and macroscopic corpus tumor area
• however, antral tumor load is similar to Il6st single mutants





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last database update
11/12/2024
MGI 6.24
The Jackson Laboratory