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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(KRT5-cre)1Xya
transgene insertion 1, Xiao Yang
MGI:3606663
Summary 8 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Ptentm2Mak/Ptentm2Mak
Tg(KRT5-cre)1Xya/0
involves: 129P2/OlaHsd MGI:3607782
cn2
Ptentm2Mak/Ptentm2Mak
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Tg(KRT5-cre)1Xya/0
involves: 129P2/OlaHsd * 129S6/SvEvTac MGI:3607778
cn3
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Tg(KRT5-cre)1Xya/0
involves: 129S6/SvEvTac MGI:3607725
cn4
Ppm1atm1Xya/Ppm1atm1Xya
Tg(KRT5-cre)1Xya/0
involves: 129S6/SvEvTac MGI:5304791
cn5
Smad2tm1Xya/Smad2tm1Xya
Tg(KRT5-cre)1Xya/0
involves: 129S6/SvEvTac MGI:5305135
cn6
Ppm1atm1.1Xya/Ppm1atm1.1Xya
Smad2tm1Xya/Smad2tm1Xya
Tg(KRT5-cre)1Xya/0
involves: 129S6/SvEvTac * FVB/N MGI:5305136
cn7
Rad9atm2Lieb/Rad9atm2Lieb
Tg(KRT5-cre)1Xya/?
involves: 129S/SvEv * C57BL/6 MGI:3809928
cn8
Rad9atm2Lieb/Rad9a+
Tg(KRT5-cre)1Xya/?
involves: 129S/SvEv * C57BL/6 MGI:3809929


Genotype
MGI:3607782
cn1
Allelic
Composition
Ptentm2Mak/Ptentm2Mak
Tg(KRT5-cre)1Xya/0
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2Mak mutation (4 available); any Pten mutation (88 available)
Tg(KRT5-cre)1Xya mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• hyperplastic outer root sheaths are seen at 3 months of age
• observed at 3 months of age




Genotype
MGI:3607778
cn2
Allelic
Composition
Ptentm2Mak/Ptentm2Mak
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Tg(KRT5-cre)1Xya/0
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2Mak mutation (4 available); any Pten mutation (88 available)
Smad4tm2.1Cxd mutation (2 available); any Smad4 mutation (48 available)
Tg(KRT5-cre)1Xya mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• some die of stomach carcinomas by 3 months of age

mortality/aging
• some die by 3 months of age due to stomach carcinomas

neoplasm
• 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

integument
• 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

cellular
• exhibit persistently proliferating follicular keratinocytes

growth/size/body
• exhibit enlarged cysts surrounded by a multilayered epithelium filled with keratinized debris or pigments




Genotype
MGI:3607725
cn3
Allelic
Composition
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Tg(KRT5-cre)1Xya/0
Genetic
Background
involves: 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Smad4tm2.1Cxd mutation (2 available); any Smad4 mutation (48 available)
Tg(KRT5-cre)1Xya mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• do not survive more than 15 months

neoplasm
• 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

integument
• 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

cellular
• increase in keratinocyte proliferation




Genotype
MGI:5304791
cn4
Allelic
Composition
Ppm1atm1Xya/Ppm1atm1Xya
Tg(KRT5-cre)1Xya/0
Genetic
Background
involves: 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ppm1atm1Xya mutation (0 available); any Ppm1a mutation (23 available)
Tg(KRT5-cre)1Xya mutation (0 available)
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

homeostasis/metabolism
• mice exhibit delayed re-epithelialization and decreased keratinocyte migration during wound healing compared with control mice

integument
• during wound healing, keratinocyte migration is decreased compared to in control mice

cellular
• during wound healing, keratinocyte migration is decreased compared to in control mice




Genotype
MGI:5305135
cn5
Allelic
Composition
Smad2tm1Xya/Smad2tm1Xya
Tg(KRT5-cre)1Xya/0
Genetic
Background
involves: 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Smad2tm1Xya mutation (0 available); any Smad2 mutation (52 available)
Tg(KRT5-cre)1Xya mutation (0 available)
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

homeostasis/metabolism
• mice exhibit accelerated re-epithelialization and enhanced keratinocyte migration in wound healing compared with control mice

integument
• during wound healing, keratinocyte migration is increased compared to in control mice

cellular
• during wound healing, keratinocyte migration is increased compared to in control mice




Genotype
MGI:5305136
cn6
Allelic
Composition
Ppm1atm1.1Xya/Ppm1atm1.1Xya
Smad2tm1Xya/Smad2tm1Xya
Tg(KRT5-cre)1Xya/0
Genetic
Background
involves: 129S6/SvEvTac * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ppm1atm1.1Xya mutation (0 available); any Ppm1a mutation (23 available)
Smad2tm1Xya mutation (0 available); any Smad2 mutation (52 available)
Tg(KRT5-cre)1Xya mutation (0 available)
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

homeostasis/metabolism
• mice exhibit accelerated re-epithelialization and enhanced keratinocyte migration in wound healing compared with control mice

integument
• during wound healing, keratinocyte migration is increased compared to control mice

cellular
• during wound healing, keratinocyte migration is increased compared to control mice




Genotype
MGI:3809928
cn7
Allelic
Composition
Rad9atm2Lieb/Rad9atm2Lieb
Tg(KRT5-cre)1Xya/?
Genetic
Background
involves: 129S/SvEv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rad9atm2Lieb mutation (0 available); any Rad9a mutation (27 available)
Tg(KRT5-cre)1Xya mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• DMBA painted onto shaved skin 2X per week for 25 weeks
• 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

cellular
• cell cycle arrest in late S phase
• in DMBA treated cells
• more double strand breaks than wild-type controls
• DMBA increases double strand breaks

pigmentation
• 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

homeostasis/metabolism
• more double strand breaks than wild-type controls
• DMBA increases double strand breaks

integument
• 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
• tumors derived from keratinocytes
• all tumor cells are conditionally deleted
• induced by DMBA treatment in about 15 weeks as compared to 27 weeks for wild-type controls
• DMBA painted onto shaved skin 2X per week for 25 weeks




Genotype
MGI:3809929
cn8
Allelic
Composition
Rad9atm2Lieb/Rad9a+
Tg(KRT5-cre)1Xya/?
Genetic
Background
involves: 129S/SvEv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rad9atm2Lieb mutation (0 available); any Rad9a mutation (27 available)
Tg(KRT5-cre)1Xya mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 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

cellular
• more double strand breaks than wild-type controls

pigmentation
• in 25% of heterozygotes compared to 13% of wild-type controls
• increased pigmentation within 2-5 weeks of tumor formation
• due to DMBA treatment

homeostasis/metabolism
• more double strand breaks than wild-type controls

integument
• 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





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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
11/19/2024
MGI 6.24
The Jackson Laboratory