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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Pard3tm1Shoh
targeted mutation 1, Shigeo Ohno
MGI:3838016
Summary 4 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Krt14tm1(cre)Wbm/Krt14+
Pard3tm1Shoh/Pard3tm1Shoh
either: FVB.129-Pard3tm1Shoh Krt14tm1(cre)Wbm or (involves: 129P2/OlaHsd * 129S4/SvJae) MGI:6258533
cn2
Krt14tm1(cre)Wbm/Krt14+
Pard3tm1Shoh/Pard3tm1Shoh
Tg(HIST1H2BB/EGFP)1Pa/0
involves: 129 * C57BL/6J MGI:6272614
cn3
Krt14tm1(cre)Wbm/Krt14+
Pard3tm1Shoh/Pard3tm1Shoh
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J MGI:6272603
cn4
Cdk4tm1.1Bbd/Cdk4tm1.1Bbd
Krt14tm1(cre)Wbm/Krt14+
Pard3tm1Shoh/Pard3tm1Shoh
Tg(Mt1-Hgf)#Lmb/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J MGI:6272611


Genotype
MGI:6258533
cn1
Allelic
Composition
Krt14tm1(cre)Wbm/Krt14+
Pard3tm1Shoh/Pard3tm1Shoh
Genetic
Background
either: FVB.129-Pard3tm1Shoh Krt14tm1(cre)Wbm or (involves: 129P2/OlaHsd * 129S4/SvJae)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krt14tm1(cre)Wbm mutation (0 available); any Krt14 mutation (36 available)
Pard3tm1Shoh mutation (0 available); any Pard3 mutation (96 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• untreated mice are viable and reach adulthood with no development of spontaneous skin tumors
• in a 2-stage DMBA/TPA skin carcinogenesis model, papilloma formation is delayed by ~3 weeks, tumor multiplicity is strongly reduced, and tumors that do form grow slower than in similarly treated wild-type controls
• in a 2-stage DMBA/TPA skin carcinogenesis model, mice show increased incidence of keratoacanthomas (KAs) with typical crater-like morphology, broad tumor base and a keratin-filled center, and tumor sizes that reach >1 cm by 22 weeks post-initiation requiring termination
• at termination, 91% of DMBA/TPA mice are KA-positive versus 27% of wild-type controls
• however, incidence of squamous cell carcinomas (SCCs) is relatively normal
• 45% of the relatively small papillomas found in in DMBA/TPA-treated mice show local invasion of tumor cells into the stroma versus 33% of the abundant larger papillomas found in wild-type controls
• 36% of keratoacanthomas (KAs) found in in DMBA/TPA-treated show local invasion into the stroma versus 0% of the KAs found in wild-type controls
• in response to DMBA/TPA treatment, papillomas that form grow slower than in wild-type controls
• at 14.5 weeks post-DMBA treatment, average papilloma size is significantly smaller than that in wild-type controls
• epidermal cell proliferation is significantly reduced, whereas epidermal apoptosis is significantly increased relative to wild-type controls
• at 22 weeks post-DMBA treatment, keratoacanthomas reach an average size of >1 cm, unlike in wild-type controls
• DMBA/TPA-treated mice show accelerated appearance of keratoacanthomas relative to wild-type controls, with KAs first detected at 7 weeks post-DMBA treatment
• in DMBA/TPA-treated mice, papilloma formation is delayed by ~3 weeks relative to wild-type controls

homeostasis/metabolism
• in a 2-stage DMBA/TPA skin carcinogenesis model, papilloma formation is delayed by ~3 weeks, tumor multiplicity is strongly reduced, and tumors that do form grow slower than in similarly treated wild-type controls
• in a 2-stage DMBA/TPA skin carcinogenesis model, mice show increased incidence of keratoacanthomas (KAs) with typical crater-like morphology, broad tumor base and a keratin-filled center, and tumor sizes that reach >1 cm by 22 weeks post-initiation requiring termination
• at termination, 91% of DMBA/TPA mice are KA-positive versus 27% of wild-type controls
• however, incidence of squamous cell carcinomas (SCCs) is relatively normal




Genotype
MGI:6272614
cn2
Allelic
Composition
Krt14tm1(cre)Wbm/Krt14+
Pard3tm1Shoh/Pard3tm1Shoh
Tg(HIST1H2BB/EGFP)1Pa/0
Genetic
Background
involves: 129 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krt14tm1(cre)Wbm mutation (0 available); any Krt14 mutation (36 available)
Pard3tm1Shoh mutation (0 available); any Pard3 mutation (96 available)
Tg(HIST1H2BB/EGFP)1Pa mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• in P58 tail whole mounts, melanocytes (MCs) show a more stubby dendritic morphology with dendritic shortening and a more spread cell body area relative to MCs in control mice




Genotype
MGI:6272603
cn3
Allelic
Composition
Krt14tm1(cre)Wbm/Krt14+
Pard3tm1Shoh/Pard3tm1Shoh
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krt14tm1(cre)Wbm mutation (0 available); any Krt14 mutation (36 available)
Pard3tm1Shoh mutation (0 available); any Pard3 mutation (96 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• in a 2-stage DMBA/TPA skin carcinogenesis model, mice show increased melanocytic hyperplasia and incidence of melanoma relative to control mice

pigmentation
• under non-tumorigenic conditions, mice show a significant increase in melanocyte number per hair follicle in back skin relative to control mice at P0, at 7 weeks, and at 4 and 12 months of age
• both the number of P-cadherin-positive keratinocytes in interfollicular epidermis and melanocyte number contacting dense P-cadherin-positive cell clusters in developing hair follicles are significantly increased relative to controls
• under non-tumorigenic conditions, newborn (P0) mice show a significant increase in interfollicular melanocytes in back skin relative to control mice
• P-cadherin-positive clusters are enlarged in interfollicular epidermis, with frequent localization of melanocytes to these compartments
• in a 2-stage DMBA/TPA skin carcinogenesis model, mice show increased melanocytic hyperplasia in the epidermis relative to control mice
• under non-tumorigenic conditions, mice show a significantly higher melanocyte number in back skin relative to control mice at P0 and all adult ages tested

integument
• under non-tumorigenic conditions, mice show a significant increase in melanocyte number per hair follicle in back skin relative to control mice at P0, at 7 weeks, and at 4 and 12 months of age
• both the number of P-cadherin-positive keratinocytes in interfollicular epidermis and melanocyte number contacting dense P-cadherin-positive cell clusters in developing hair follicles are significantly increased relative to controls
• under non-tumorigenic conditions, newborn (P0) mice show a significant increase in interfollicular melanocytes in back skin relative to control mice
• P-cadherin-positive clusters are enlarged in interfollicular epidermis, with frequent localization of melanocytes to these compartments

homeostasis/metabolism
• in a 2-stage DMBA/TPA skin carcinogenesis model, mice show increased melanocytic hyperplasia and incidence of melanoma relative to control mice




Genotype
MGI:6272611
cn4
Allelic
Composition
Cdk4tm1.1Bbd/Cdk4tm1.1Bbd
Krt14tm1(cre)Wbm/Krt14+
Pard3tm1Shoh/Pard3tm1Shoh
Tg(Mt1-Hgf)#Lmb/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdk4tm1.1Bbd mutation (0 available); any Cdk4 mutation (57 available)
Krt14tm1(cre)Wbm mutation (0 available); any Krt14 mutation (36 available)
Pard3tm1Shoh mutation (0 available); any Pard3 mutation (96 available)
Tg(Mt1-Hgf)#Lmb mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• at 8-15 weeks after DMBA treatment, mice exhibit significantly increased melanoma multiplicity relative to control mice, with primary melanomas invading the dermis and showing tumor-associated angiogenesis
• less than 15 weeks after DMBA treatment, mice show increased incidence of distal melanoma metastases in the lungs relative to control mice (57.1% versus 16.7%)
• in DMBA-treated mice, primary melanomas show an increased proliferative index, with a significantly higher number of PCNAhigh melanoma cells relative to control mice, consistent with increased melanoma multiplicity

homeostasis/metabolism
• at 8-15 weeks after DMBA treatment, mice exhibit significantly increased melanoma multiplicity relative to control mice, with primary melanomas invading the dermis and showing tumor-associated angiogenesis





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last database update
04/16/2024
MGI 6.23
The Jackson Laboratory