Analysis Tools|
Allele Symbol Allele Name Allele ID |
Tg(KRT5-rtTA)1Glk transgene insertion 1, Adam Glick MGI:3575756 |
| Summary |
9 genotypes |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at P50 doxycycline-treated mice exhibit loss of bulge stem cells unlike in control mice
• however, bulge stem cells are present at P20 and P22
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• in doxycycline-treated mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• doxycycline-treated mice retain hair follicle stem cells in early telogen and anagen
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• hair phenotype in doxycycline-treated mice appears more slowly than in Dicer1tm1Smr/Dicer1tm1Smr Tg(KRT5-rtTA)1Glk Tg(tetO-cre)1Jaw mice
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• failure of hair regrowth in doxycycline-treated mice
• failure of regression at P20 in doxycycline-treated mice and remained in an abnormal growth phase
• following hair plucking, doxycycline-treated mice fail to sustain hair growth unlike control mice
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• external hair becomes wavy between P12 and P14 in doxycycline-treated mice
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• in doxycycline-treated mice likely due to matrix cell apoptosis
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• at P17 in doxycycline-treated mice after degradation begins
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• fewer differentiation cell in doxycycline-treated mice following plucking-induced anagen initiation
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• with extrusion of abnormally keratinized cellular material in doxycycline-treated mice
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• in doxycycline-treated mice following plucking-induced anagen initiation
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• failure of catagen in doxycycline-treated mice
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• failure of regression at P20 in doxycycline-treated mice
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• by P20, doxycycline-treated mice exhibit thickened interfollicular epidermis compared with control mice
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• mice treated with doxycycline exhibit a temporary phenotype of dry scaly skin that is resolved in an anterior-posterior direction
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• mice treated with doxycycline exhibit a temporary phenotype of dry scaly skin that is resolved in an anterior-posterior direction
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• doxycycline-treated mice exhibit matrix cell apoptosis with DNA damage response unlike in control mice
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• in doxycycline-treated mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• doxycycline-treated mice retain hair follicle stem cells in early telogen and anagen
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• hair phenotype in doxycycline-treated mice appears more rapidly than in Droshatm1Litt/Droshatm1Litt Tg(KRT5-rtTA)1Glk Tg(tetO-cre)1Jaw mice
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• failure of hair regrowth in doxycycline-treated mice
• failure of regression at P20 in doxycycline-treated mice and remained in an abnormal growth phase
• following hair plucking, doxycycline-treated mice fail to sustain hair growth unlike control mice
|
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• external hair becomes wavy between P12 and P14 in doxycycline-treated mice
|
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• in doxycycline-treated mice likely due to matrix cell apoptosis
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• at P17 in doxycycline-treated mice after degradation begins
|
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• fewer differentiation cell in doxycycline-treated mice following plucking-induced anagen initiation
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• at P59 doxycycline-treated mice exhibit loss of bulge stem cells unlike in control mice
• however, bulge stem cells are present at P20 and P22
|
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• with extrusion of abnormally keratinized cellular material in doxycycline-treated mice
|
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• in doxycycline-treated mice following plucking-induced anagen initiation
|
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• failure of catagen in doxycycline-treated mice
|
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• failure of regression at P20 in doxycycline-treated mice
|
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• by P20, doxycycline-treated mice exhibit thickened interfollicular epidermis compared with control mice
|
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• mice treated with doxycycline exhibit a temporary phenotype of dry scaly skin that is resolved in an anterior-posterior direction
|
|
• mice treated with doxycycline exhibit a temporary phenotype of dry scaly skin that is resolved in an anterior-posterior direction
|
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• doxycycline-treated mice exhibit matrix cell apoptosis with DNA damage response unlike in control mice
|
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• in doxycycline-treated mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• dox treated mutants develop autoimmune hemolytic anemia
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• mature follicular B cells in doxycycline (dox) treated mutants display features of polyclonal activation, including down-regulation of CD21/CD35 expression, elevated CD23 and MHC class II expression, increased cell size and increased mitogenic responses
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• following polyclonal stimulation in vitro, primary B cells from dox treated mutants exhibit higher levels of [3H] thymidine incorporation, indicating increased proliferation potential
• following anti-IgM and LPS stimulation, primary B cells from dox treated mutants, exhibit higher levels of BrdU incorporation, indicating increased proliferation potential
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• dox treated mutants exhibit an increase in serum IL-4 levels
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• following dox treatment, mutants show the presence of anti-RBC-specific autoantibodies
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• dox treated mutants develop autoimmune hemolytic anemia
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• following dox treatment, mutants show a decrease in hematocrit corresponding with the presence of anti-RBC-specific autoantibodies, consistent with onset of hemolytic anemia
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• mature follicular B cells in doxycycline (dox) treated mutants display features of polyclonal activation, including down-regulation of CD21/CD35 expression, elevated CD23 and MHC class II expression, increased cell size and increased mitogenic responses
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• following polyclonal stimulation in vitro, primary B cells from dox treated mutants exhibit higher levels of [3H] thymidine incorporation, indicating increased proliferation potential
• following anti-IgM and LPS stimulation, primary B cells from dox treated mutants, exhibit higher levels of BrdU incorporation, indicating increased proliferation potential
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• dox treated mutants exhibit an increase in serum IL-4 levels
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• following polyclonal stimulation in vitro, primary B cells from dox treated mutants exhibit higher levels of [3H] thymidine incorporation, indicating increased proliferation potential
• following anti-IgM and LPS stimulation, primary B cells from dox treated mutants, exhibit higher levels of BrdU incorporation, indicating increased proliferation potential
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| autoimmune hemolytic anemia | DOID:718 |
OMIM:205700 |
J:182756 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mutants treated with dox for 3 weeks exhibit dermal infiltration mostly of mast cells and eosinophils
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• mutants treated with doxycycline (dox) for 3 weeks exhibit dermal infiltration mostly of mast cells and eosinophils
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• mutants treated with dox for 3 weeks exhibit epidermal thickening
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• dox treated mice exhibit little or no serum IgE
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• mutants treated with dox for 3 weeks exhibit dermal infiltration mostly of mast cells and eosinophils
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• dox treated mice exhibit little or no serum IgE
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• by 5 weeks of doxycycline (dox) treatment, lesional skin shows characteristic changes of eczematous inflammation including spongiosis
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• mutants treated with doxycycline (dox) to induce expression of Tslp develop skin disease beginning at about 2-3 weeks of dox treatment
• dox treated mutants exhibit dermal infiltrates containing lymphocytes, macrophages, mast cells, and eosinophils
• however, inflammation is not seen in the small intestine or colon
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• by 5 weeks of dox treatment, lesional skin shows characteristic changes of eczematous inflammation including hyperkeratosis
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• by 5 weeks of dox treatment, lesional skin shows characteristic changes of eczematous inflammation including acanthosis
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• seen in dox treated mutants
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• dox treated mutants exhibit skin lesions consisting of mild erythema at 2 weeks of dox treatment with progression to eczematous-like changes, including erythema, crusting, and erosions, by 3-4 weeks of dox treatment
• skin lesions are most common on the snout, postauricular region, nape of the neck and upper back
• less commonly, lesions are seen on the anterior neck and hind legs
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• dox treated mutants exhibit splenomegaly
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• dox treated mutants exhibit an increase in the frequency of and absolute numbers of IL-4 producing Th2 CD4+ T cells in both the spleens and lymph nodes
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• in dox treated mutants
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• in dox treated mutants
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• in dox treated mutants
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• dox treated mutants exhibit an increase in Th2 cytokines in effected skin
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• dox treated mutants exhibit a 14-fold increase in IL-4 producing cells in the skin-draining lymph nodes and an 18-fold increase in the intestinal mesenteric lymph nodes
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• dox treated mutants exhibit lymphadenopathy
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• a few dox treated mice exhibit conjunctivitis
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• mutants treated with doxycycline (dox) to induce expression of Tslp develop skin disease beginning at about 2-3 weeks of dox treatment
• dox treated mutants exhibit dermal infiltrates containing lymphocytes, macrophages, mast cells, and eosinophils
• however, inflammation is not seen in the small intestine or colon
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• dox treated mutants exhibit splenomegaly
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• dox treated mutants exhibit an increase in the frequency of and absolute numbers of IL-4 producing Th2 CD4+ T cells in both the spleens and lymph nodes
|
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• in dox treated mutants
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• in dox treated mutants
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• in dox treated mutants
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• by 5 weeks of doxycycline (dox) treatment, lesional skin shows characteristic changes of eczematous inflammation including spongiosis
|
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• dox treated mutants exhibit an increase in Th2 cytokines in effected skin
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• a few dox treated mice exhibit conjunctivitis
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• dox treated mutants exhibit splenomegaly
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| atopic dermatitis | DOID:3310 |
OMIM:603165 OMIM:PS603165 |
J:100506 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• of ovalbumin-specific CD4 T cells in doxycycline-treated mice unlike when cells are transferred into control mice
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• airway inflammation in doxycycline-treated mice treated intranasally with ovalbumin
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• eczematous inflammation in the skin of doxycycline- and anti-mTSLP antibody-treated mice
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• eczematous inflammation in the skin of doxycycline- and anti-mTSLP antibody-treated mice
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• airway inflammation in doxycycline-treated mice treated intranasally with ovalbumin
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• of ovalbumin-specific CD4 T cells in doxycycline-treated mice unlike when cells are transferred into control mice
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• of ovalbumin-specific CD4 T cells in doxycycline-treated mice unlike when cells are transferred into control mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• doxycycline- and anti-mTSLP antibody-treated mice do not exhibit eczematous inflammation
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| N |
• doxycycline- and anti-mTSLP antibody-treated mice do not exhibit eczematous inflammation
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• double-transgenic mice with normal morphology are born at expected ratios when no doxycycline treatment is given to the dam
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• epidermis of weaning-aged mice dosed with doxycycline displays a variable neutrophilic infiltrate characterized by microabcesses within and above cornified layers
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• weaning-aged mice dosed with doxycycline develop dermatitis on scalp and shoulders, as well as ventral surface, within 3-4 weeks; dermatitis extends caudally with time
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• treatment with doxycycline induces keratinocyte apoptosis
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• cell proliferation in hyperplastic dermis of doxycycline-treated animals is elevated
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• when adult mice undergo depilation and receive doxycycline treatment, cell proliferation is significantly reduced compared to mice which receive no doxycycline or single-transgenic controls
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• treatment with doxycycline induces keratinocyte apoptosis
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• epidermis of weaning-aged mice dosed with doxycycline displays a variable neutrophilic infiltrate characterized by microabcesses within and above cornified layers
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• weaning-aged mice dosed with doxycycline develop dermatitis on scalp and shoulders, as well as ventral surface, within 3-4 weeks; dermatitis extends caudally with time
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• weaning-aged mice dosed with doxycycline display progressive hair loss within 3-4 weeks
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• in weaning-aged mice dosed with doxycycline, many hair follicles appear hyperplastic with abnormal morphologies
• in animals treated with doxycycline, nearly all hair follicles have proliferating cells in the outer root sheath particularly in the infundibular region
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• hair follicle density is significantly reduced in weaning-aged mice dosed with doxycycline
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• treatment of animals with doxycycline causes keratinocytes to undergo growth arrest
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• increased cellularity is observed in weaning-aged mice dosed with doxycycline
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• significant thickening is observed in weaning-aged mice dosed with doxycycline
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• weaning-aged mice dosed with doxycycline develop hyperkeratosis within 3-4 weeks
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• epidermis of affected mice (weanlings treated with doxycycline) becomes acanthotic
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• epidermis of affected mice (weanlings treated with doxycycline) exhibits hyperplasia
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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 11/12/2024 MGI 6.24 |
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