Analysis Tools
integument
|
• hyperplastic outer root sheaths are seen at 3 months of age
|
|
• observed at 3 months of age
|
|
Allele Symbol Allele Name Allele ID |
Tg(KRT5-cre)1Xya transgene insertion 1, Xiao Yang MGI:3606663 |
||||||||||||||||||||||||||||||||||||
| Summary |
8 genotypes
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• hyperplastic outer root sheaths are seen at 3 months of age
|
|
• observed at 3 months of age
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• some die of stomach carcinomas by 3 months of age
|
|
• some die by 3 months of age due to stomach carcinomas
|
|
• some die of stomach carcinomas by 3 months of age
|
|
• tumor formation is accelerated in comparison to conditional keratinocyte targeted Smad4tm2.1Cxd or Ptentm2Mak mutant mice
|
|
• develop visible squamous papillomas on their backs at 2 months of age
|
|
• some die of stomach carcinomas by 3 months of age
|
|
• tumor formation is accelerated in comparison to conditional keratinocyte targeted Smad4tm2.1Cxd or Ptentm2Mak mutant mice
|
|
• exhibit persistently proliferating follicular keratinocytes
|
|
• exhibit enlarged cysts surrounded by a multilayered epithelium filled with keratinized debris or pigments
|
|
• exhibit obvious hair loss 2 months after birth, about 1 month earlier than conditional keratinocyte targeted Smad4tm2.1Cxd mutant mice
|
|
• outer root sheath is thicker at P18
|
|
• hair follicles fail to go into catagen stage, indicating blocked regression
|
|
• hair follicles have significantly more proliferating cells at P18 than conditional keratinocyte targeted Ptentm2Mak mutant mice
|
|
• thickened epidermis is observed at P18
|
|
• tumor formation is accelerated in comparison to conditional keratinocyte targeted Smad4tm2.1Cxd or Ptentm2Mak mutant mice
|
|
• develop visible squamous papillomas on their backs at 2 months of age
|
|
• exhibit persistently proliferating follicular keratinocytes
|
|
• exhibit enlarged cysts surrounded by a multilayered epithelium filled with keratinized debris or pigments
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• do not survive more than 15 months
|
|
• start to develop skin tumors around 5 months of age and by 12 months of age, 70% exhibit visible tumors
|
|
• most are well-differentiated squamous cell carcinomas and squamous papillomas
|
|
• most are well-differentiated squamous cell carcinomas and squamous papillomas
|
|
• exhibit progressive hair loss that is first evident at P20, is obvious at 3 months of age, and generalized alopecia is seen by 7 months of age
|
|
• cysts are seen in the hypodermis
|
|
• increase in cell proliferation in hair follicle compared to controls at P25
• hair follicles are disordered and hypertrophied
|
|
• the outer root sheath is abnormally thick and exhibits an increase in cell proliferation in the first anagen at P15
|
|
• size of hair follicles is increased at 2 months of age
|
|
• hair follicles fail to regress and persist in an abnormal anagen phase; by P30 when a new anagen phase starts in controls, homozygotes exhibit thickened and distored follicles
• lower number of apoptotic cells in the hair bulb of early catagen hair follicles
|
|
• basal layer of the epidermis is thickened
|
|
• severe hyperkeratosis in the esophagus at 7 months of age
|
|
• number of keratinocytes is increased in the epidermis and hair follicles
|
|
• increase in epidermal proliferation
|
|
• black and white cysts are seen through out the skin surface
|
|
• skin is thick and stiff
|
|
• start to develop skin tumors around 5 months of age and by 12 months of age, 70% exhibit visible tumors
|
|
• most are well-differentiated squamous cell carcinomas and squamous papillomas
|
|
• response of keratinocytes to growth inhibition by TGF-beta1 is impaired
|
|
• increase in keratinocyte proliferation
|
|
• increase in keratinocyte proliferation
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Delayed re-epithelialization during wound healing in Ppm1atm1Xya/Ppm1atm1Xya Tg(KRT5-cre)1Xya/0 mice
|
• mice exhibit delayed re-epithelialization and decreased keratinocyte migration during wound healing compared with control mice
|
|
• during wound healing, keratinocyte migration is decreased compared to in control mice
|
|
• during wound healing, keratinocyte migration is decreased compared to in control mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Accelerated re-epithelialization during wound healing in Smad2tm1Xya/Smad2tm1Xya Tg(KRT5-cre)1Xya/0 mice
|
• mice exhibit accelerated re-epithelialization and enhanced keratinocyte migration in wound healing compared with control mice
|
|
• during wound healing, keratinocyte migration is increased compared to in control mice
|
|
• during wound healing, keratinocyte migration is increased compared to in control mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Re-epithelialization rate is accelerated in Smad2tm1Xya/Smad2tm1Xya Ppm1atm1.1Xya/Ppm1atm1.1Xya Tg(KRT5-cre)1Xya/0 mice
|
• mice exhibit accelerated re-epithelialization and enhanced keratinocyte migration in wound healing compared with control mice
|
|
• during wound healing, keratinocyte migration is increased compared to control mice
|
|
• during wound healing, keratinocyte migration is increased compared to control mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• induced by DMBA treatment in about 15 weeks as compared to 27 weeks for wild-type controls
• tumors derived from keratinocytes
• all tumor cells are conditionally deleted
• DMBA painted onto shaved skin 2X per week for 25 weeks
|
|
• cell cycle arrest in late S phase
|
|
• in DMBA treated cells
|
|
• more double strand breaks than wild-type controls
• DMBA increases double strand breaks
|
|
• due to DMBA treatment
• in 81% of homozygotes as compared to 13% of wild-type controls
• increased pigmentation within 2-5 weeks of tumor formation
|
|
• more double strand breaks than wild-type controls
• DMBA increases double strand breaks
|
|
• due to DMBA treatment
• in 81% of homozygotes as compared to 13% of wild-type controls
• increased pigmentation within 2-5 weeks of tumor formation
|
|
• induced by DMBA treatment in about 15 weeks as compared to 27 weeks for wild-type controls
• tumors derived from keratinocytes
• all tumor cells are conditionally deleted
• DMBA painted onto shaved skin 2X per week for 25 weeks
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• induced by DMBA treatment in about 25 weeks for heterozygotes compared to 27 weeks for wild-type controls
• tumors derived from keratinocytes
• all tumor cells are conditionally deleted
• DMBA painted onto shaved skin 2X per week for 25 weeks
|
|
• more double strand breaks than wild-type controls
|
|
• in 25% of heterozygotes compared to 13% of wild-type controls
• increased pigmentation within 2-5 weeks of tumor formation
• due to DMBA treatment
|
|
• more double strand breaks than wild-type controls
|
|
• in 25% of heterozygotes compared to 13% of wild-type controls
• increased pigmentation within 2-5 weeks of tumor formation
• due to DMBA treatment
|
|
• induced by DMBA treatment in about 25 weeks for heterozygotes compared to 27 weeks for wild-type controls
• tumors derived from keratinocytes
• all tumor cells are conditionally deleted
• DMBA painted onto shaved skin 2X per week for 25 weeks
|
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
||
|
Citing These Resources Funding Information Warranty Disclaimer, Privacy Notice, Licensing, & Copyright Send questions and comments to User Support. |
last database update 05/07/2024 MGI 6.23 |
|
|
|
||