Phenotypes associated with this allele

• Allele Symbol: Krt14⁺
• Allele Name: wild type
• Allele ID: MGI:2431151
• Summary: 20 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
ht1	Krt14^tm1.1(KOMP)Vlcg/Krt14^+	C57BL/6N-Krt14^tm1.1(KOMP)Vlcg/Ucd	MGI:6678934
ht2	Krt14^tm2Der/Krt14^+	involves: 129X1/SvJ	MGI:2653131
cn3	Arpc4^tm1c(EUCOMM)Wtsi/Arpc4^tm1c(EUCOMM)Wtsi Krt14^tm1(cre)Wbm/Krt14^+	B6.Cg-Arpc4^tm1c(EUCOMM)Wtsi Krt14^tm1(cre)Wbm	MGI:6115481
cn4	Krt14^tm1(cre)Wbm/Krt14^+ Pard3^tm1Shoh/Pard3^tm1Shoh	either: FVB.129-Pard3^tm1Shoh Krt14^tm1(cre)Wbm or (involves: 129P2/OlaHsd * 129S4/SvJae)	MGI:6258533
cn5	Krt14^tm1(cre)Wbm/Krt14^+ Pard3^tm1Shoh/Pard3^tm1Shoh Tg(HIST1H2BB/EGFP)1Pa/0	involves: 129 * C57BL/6J	MGI:6272614
cn6	Ctnnb1^tm4Wbm/Ctnnb1^tm4Wbm Krt14^tm1(cre)Wbm/Krt14^+	involves: 129P2/OlaHsd	MGI:5547809
cn7	Zbtb17^tm1Cksn/Zbtb17^tm1Cksn Krt14^tm1(cre)Wbm/Krt14^+	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ	MGI:3721959
cn8	Zbtb17^tm1Cksn/Zbtb17^tm1.1Cksn Krt14^tm1(cre)Wbm/Krt14^+	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ	MGI:3721960
cn9	Krt14^tm1(cre)Wbm/Krt14^+ Pard3^tm1Shoh/Pard3^tm1Shoh	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J	MGI:6272603
cn10	Cdk4^tm1.1Bbd/Cdk4^tm1.1Bbd Krt14^tm1(cre)Wbm/Krt14^+ Pard3^tm1Shoh/Pard3^tm1Shoh Tg(Mt1-Hgf)#Lmb/0	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J	MGI:6272611
cn11	Bmpr1a^tm2.1Bhr/Bmpr1a^tm2.1Bhr Krt14^tm1.1(cre)Wbm/Krt14^+	involves: 129P2/OlaHsd * 129S7/SvEvBrd	MGI:5508225
cn12	Bmpr1a^tm2.1Bhr/Bmpr1a^tm2.1Bhr Ctnnb1^tm1Mmt/Ctnnb1^+ Krt14^tm1.1(cre)Wbm/Krt14^+	involves: 129P2/OlaHsd * 129S7/SvEvBrd * 129X1/SvJ	MGI:5508218
cn13	Ctnnb1^tm1Mmt/Ctnnb1^+ Krt14^tm1.1(cre)Wbm/Krt14^+	involves: 129P2/OlaHsd * 129X1/SvJ	MGI:5508224
cn14	Wls^tm1.1Arte/Wls^tm1.1Arte Krt14^tm1(cre)Wbm/Krt14^+	involves: 129P2/OlaHsd * C57BL/6	MGI:5547811
cn15	Ctnnb1^tm4Wbm/Ctnnb1^tm4Wbm Krt14^tm1(cre)Wbm/Krt14^+	involves: 129P2/OlaHsd * C57BL/6	MGI:2673246
cn16	Ctnnb1^tm4Wbm/Ctnnb1^tm4Wbm Krt14^tm1.1(cre)Wbm/Krt14^+	involves: 129P2/OlaHsd * C57BL/6	MGI:2673250
cn17	Krt14^tm1.1(cre)Wbm/Krt14^+ Tg(KRT14-Snai1)1Efu/0 Trp53^tm1Brn/Trp53^tm1Brn	involves: 129P2/OlaHsd * CD-1	MGI:6196149
cn18	Itga3^tm1Son/Itga3^tm1Son Krt14^tm1(cre)Wbm/Krt14^+	involves: 129P2/OlaHsd * FVB/N	MGI:3836769
cn19	Krt14^tm1Der/Krt14^+ Tg(KRT14-cre/PGR)1Der/?	involves: 129X1/SvJ * FVB * ICR	MGI:3812200
cn20	Krt14^tm1Der/Krt14^+ Tg(KRT5-cre/PGR)1Der/?	involves: 129X1/SvJ * FVB * ICR	MGI:3812201

Genotype
MGI:6678934

ht1

• Allelic Composition: Krt14^{tm1.1(KOMP)Vlcg}/Krt14⁺
• Genetic Background: C57BL/6N-Krt14^{tm1.1(KOMP)Vlcg}/Ucd
• Cell Lines: 12488A-C5

Data Sources

IMPC Data for Krt14

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

cardiovascular system

hemorrhage ( J:211773 )

IMPC - UCD

embryo

spina bifida ( J:211773 )

IMPC - UCD

nervous system

spina bifida ( J:211773 )

IMPC - UCD

Genotype
MGI:2653131

ht2

• Allelic Composition: Krt14^tm2Der/Krt14⁺
• Genetic Background: involves: 129X1/SvJ

Blistering on the left front leg and abdomen of Krt14^tm2Der/Krt14⁺ pups

mortality/aging

postnatal lethality, complete penetrance ( J:67320 )

• mutants die a week after birth due to severe blistering

integument

abnormal keratinocyte morphology ( J:67320 )

• basal keratinocytes contain keratin clumps and short keratin filaments, in contrast to wild type keratinocytes which contain long keratin filaments

• however, normal keratin filaments are seen in the suprabasal layer of the epidermis

blistering ( J:67320 )

• pups develop large blisters on their forelimbs and trunk

• lymphocyte infiltration is seen in blistering areas

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
epidermolysis bullosa simplex Dowling-Meara type		DOID:0060735	OMIM:131760	J:67320

Genotype
MGI:6115481

cn3

• Allelic Composition: Arpc4^{tm1c(EUCOMM)Wtsi}/Arpc4^{tm1c(EUCOMM)Wtsi}; Krt14^tm1(cre)Wbm/Krt14⁺
• Genetic Background: B6.Cg-Arpc4^{tm1c(EUCOMM)Wtsi} Krt14^tm1(cre)Wbm
• Cell Lines: EPD0058_1_A11

integument

abnormal keratinocyte differentiation ( J:253986 )

• molecular analysis revealed disrupted keratinocyte differentiation

absent sebaceous gland ( J:253986 )

• at P7, hair follicles in psoriasis-like lesions often lack the sebaceous gland

abnormal head skin morphology ( J:253986 )

• at P1, local thickening of the epidermis, mainly the cornified layer, and scattered ghost (anucleated) cells are mostly evident in the head region

alopecia ( J:253986 )

• at P5, pups exhibit uneven skin thickening with alopecic areas

• at P7, hair follicles in psoriasis-like lesions often lack the shaft

sparse hair ( J:253986 )

• at P5, body and extremities show poorly furred skin

decreased hair follicle number ( J:253986 )

• at P7, hair follicles in psoriasis-like lesions are rare

hyperkeratosis ( J:253986 )

• at P7, the cornified layer is abnormally thickened

parakeratosis ( J:253986 )

• at P7, the thickened cornified layer is characterized by the presence of nuclei and microabscesses

acanthosis ( J:253986 )

• at P7, the epidermal squamous cells exhibit hyperplasia (acanthosis)

thick epidermis ( J:253986 )

• at P1, local thickening of the epidermis, mainly the cornified layer, are mostly evident in the head region

• at P5, body and extremities show unevenly thickened skin

abnormal skin appearance ( J:253986 )

• at P5, pups exhibit abnormal skin appearance with uneven thickening accompanied by alopecic areas

dry skin ( J:253986 )

• at P5, body and extremities show dry skin

scaly skin ( J:253986 )

• over time, psoriasis-like lesions acquire an ichthyosis-like appearance

skin lesions ( J:253986 )

• initial skin lesions are detected microscopically at P1; mice have to be euthanized by P21 due to the severity of skin lesions

psoriasis ( J:253986 )

• at P1, local thickening of the epidermis, mainly the cornified layer, and scattered ghost (anucleated) cells are mostly evident in the head region

• initial skin lesions develop progressively into macroscopic psoriasis-like plaques

• psoriasis-like lesions are variable in size and usually more severe in the dorsal than in the ventral trunk, extremities and head

• over time, psoriasis-like lesions acquire an ichthyosis-like appearance

• psoriatic epidermis exhibits hyperactivation of transcription factor Nrf2 and decreased F-actin levels

• however, mice do not exhibit any outside-in epidermal permeability barrier defects

abnormal skin physiology ( J:253986 )

• skin lesions show increased Ki67 positivity in both the basal and the suprabasal epidermal layers

• at P4, the mutant epidermis shows increased nuclear Nrf2 levels; whereas the number of Nrf2-positive interfollicular keratinocytes declines with age in wild-type epidermis, Nrf2 expression remains ubiquitous in psoriasis-like lesions at P14, indicating Nrf2 hyperactivation

dermatitis ( J:253986 )

• at P7, P14 and P21, inflammatory infiltrations mainly consisting of lymphocytic cells are detected in the dermis

cellular

abnormal keratinocyte differentiation ( J:253986 )

• molecular analysis revealed disrupted keratinocyte differentiation

endocrine/exocrine glands

absent sebaceous gland ( J:253986 )

• at P7, hair follicles in psoriasis-like lesions often lack the sebaceous gland

growth/size/body

abnormal head skin morphology ( J:253986 )

• at P1, local thickening of the epidermis, mainly the cornified layer, and scattered ghost (anucleated) cells are mostly evident in the head region

immune system

dermatitis ( J:253986 )

• at P7, P14 and P21, inflammatory infiltrations mainly consisting of lymphocytic cells are detected in the dermis

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
psoriasis		DOID:8893	OMIM:PS177900	J:253986

Genotype
MGI:6258533

cn4

• Allelic Composition: Krt14^tm1(cre)Wbm/Krt14⁺; Pard3^tm1Shoh/Pard3^tm1Shoh
• Genetic Background: either: FVB.129-Pard3^tm1Shoh Krt14^tm1(cre)Wbm or (involves: 129P2/OlaHsd * 129S4/SvJae)

neoplasm

neoplasm ( J:192905 )

N • untreated mice are viable and reach adulthood with no development of spontaneous skin tumors

decreased incidence of tumors by chemical induction ( J:192905 )

• 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

increased incidence of tumors by chemical induction ( J:192905 )

• 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

increased metastatic potential ( J:192905 )

• 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

decreased tumor growth/size ( J:192905 )

• 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

increased tumor growth/size ( J:192905 )

• at 22 weeks post-DMBA treatment, keratoacanthomas reach an average size of >1 cm, unlike in wild-type controls

decreased tumor latency ( J:192905 )

• DMBA/TPA-treated mice show accelerated appearance of keratoacanthomas relative to wild-type controls, with KAs first detected at 7 weeks post-DMBA treatment

increased tumor latency ( J:192905 )

• in DMBA/TPA-treated mice, papilloma formation is delayed by ~3 weeks relative to wild-type controls

homeostasis/metabolism

decreased incidence of tumors by chemical induction ( J:192905 )

• 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

increased incidence of tumors by chemical induction ( J:192905 )

• 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

cn5

• Allelic Composition: Krt14^tm1(cre)Wbm/Krt14⁺; Pard3^tm1Shoh/Pard3^tm1Shoh; Tg(HIST1H2BB/EGFP)1Pa/0
• Genetic Background: involves: 129 * C57BL/6J

pigmentation

abnormal melanocyte morphology ( J:240961 )

• 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:5547809

cn6

• Allelic Composition: Ctnnb1^tm4Wbm/Ctnnb1^tm4Wbm; Krt14^tm1(cre)Wbm/Krt14⁺
• Genetic Background: involves: 129P2/OlaHsd

immune system

increased neutrophil cell number ( J:202499 )

• enhanced infiltration in the skin

decreased gamma-delta T cell number ( J:202499 )

• decrease in gamma-delta TCR+ T cells (dendritic epidermal T cells) in the skin

hematopoietic system

increased neutrophil cell number ( J:202499 )

• enhanced infiltration in the skin

decreased gamma-delta T cell number ( J:202499 )

• decrease in gamma-delta TCR+ T cells (dendritic epidermal T cells) in the skin

Genotype
MGI:3721959

cn7

• Allelic Composition: Zbtb17^tm1Cksn/Zbtb17^tm1Cksn; Krt14^tm1(cre)Wbm/Krt14⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ

pigmentation

darkened coat color ( J:123966 )

• at one year of age mice have darker coat and skin than wild-type mice

• in areas of substantial hair loss a black dot-like area is visible

• light-tipped zigzag hairs are decreased in number

abnormal hair follicle melanocyte morphology ( J:123966 )

• back skin displays abnormal content distribution of melanin

• in areas of substantial hair loss a black dot-like area is visible

• mice exhibit focal areas in the dermis and subcutis around hair follicles with high melanin content

integument

increased keratinocyte proliferation ( J:123966 )

• keratinocyte located at the orifice of the hair funnel exhibit increased proliferation

• proliferation of keratinocyte in the anagen but not the catagen of the hair cycle is increased

abnormal coat/ hair morphology ( J:123966 )

darkened coat color ( J:123966 )

• at one year of age mice have darker coat and skin than wild-type mice

• in areas of substantial hair loss a black dot-like area is visible

• light-tipped zigzag hairs are decreased in number

abnormal hair follicle melanocyte morphology ( J:123966 )

• back skin displays abnormal content distribution of melanin

• in areas of substantial hair loss a black dot-like area is visible

• mice exhibit focal areas in the dermis and subcutis around hair follicles with high melanin content

focal dorsal hair loss ( J:123966 )

• mice experience hair loss on the back skin without a reduction in the number of hair follicles

sparse hair ( J:123966 )

• hair density is decreased

rough coat ( J:123966 )

• 100% of mice have rough fur

• initially rough areas appear in stripes

decreased curvature of zigzag hairs ( J:123966 )

decreased zigzag hair amount ( J:123966 )

• only 24% to 54% of hairs are of the zigzag type compared to 70% in wild-type mice

abnormal hair follicle morphology ( J:123966 )

• hair follicle length is highly variable relative to in wild-type mice

• cyst-like hair follicles containing hair remnants are observed in some areas

• cystic alterations occur in the upper part of the follicle and epithelium of the cyst-like structure is continuous with the epidermis

• the number of hair follicles extending into the subcutis is increased relative to in wild-type mice

• catagen during the hair cycle is delayed

• at one year of age, numerous back skin hair follicles are thickened

abnormal hair follicle orientation ( J:123966 )

• the orientation of hair follicles is altered relative to in wild-type mice

abnormal epidermal layer morphology ( J:123966 )

• the number of interfollicular epidermal layers is increased

hyperkeratosis ( J:123966 )

cellular

increased keratinocyte proliferation ( J:123966 )

• keratinocyte located at the orifice of the hair funnel exhibit increased proliferation

• proliferation of keratinocyte in the anagen but not the catagen of the hair cycle is increased

Genotype
MGI:3721960

cn8

• Allelic Composition: Zbtb17^tm1Cksn/Zbtb17^tm1.1Cksn; Krt14^tm1(cre)Wbm/Krt14⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ

integument

rough coat ( J:123966 )

• 100% of mice have rough fur

• initially rough areas appear in stripes

Genotype
MGI:6272603

cn9

• Allelic Composition: Krt14^tm1(cre)Wbm/Krt14⁺; Pard3^tm1Shoh/Pard3^tm1Shoh
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J

neoplasm

increased incidence of tumors by chemical induction ( J:240961 )

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

pigmentation

abnormal hair follicle melanocyte morphology ( J:240961 )

• 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

abnormal epidermal melanocyte morphology ( J:240961 )

• 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

increased melanocyte number ( J:240961 )

• 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

abnormal hair follicle melanocyte morphology ( J:240961 )

• 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

abnormal epidermal melanocyte morphology ( J:240961 )

• 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

increased incidence of tumors by chemical induction ( J:240961 )

• 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

cn10

• Allelic Composition: Cdk4^tm1.1Bbd/Cdk4^tm1.1Bbd; Krt14^tm1(cre)Wbm/Krt14⁺; Pard3^tm1Shoh/Pard3^tm1Shoh; Tg(Mt1-Hgf)#Lmb/0
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J

neoplasm

increased incidence of tumors by chemical induction ( J:240961 )

• 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

increased metastatic potential ( J:240961 )

• 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%)

increased tumor growth/size ( J:240961 )

• in DMBA-treated mice, primary melanomas show an increased proliferative index, with a significantly higher number of PCNA^high melanoma cells relative to control mice, consistent with increased melanoma multiplicity

homeostasis/metabolism

increased incidence of tumors by chemical induction ( J:240961 )

• 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

Genotype
MGI:5508225

cn11

• Allelic Composition: Bmpr1a^tm2.1Bhr/Bmpr1a^tm2.1Bhr; Krt14^{tm1.1(cre)Wbm}/Krt14⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S7/SvEvBrd

neoplasm

neoplasm ( J:199091 )

N • mice do not develop salivary gland squamous cell carcinoma

Genotype
MGI:5508218

cn12

• Allelic Composition: Bmpr1a^tm2.1Bhr/Bmpr1a^tm2.1Bhr; Ctnnb1^tm1Mmt/Ctnnb1⁺; Krt14^{tm1.1(cre)Wbm}/Krt14⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S7/SvEvBrd * 129X1/SvJ

mortality/aging

decreased tumor-free survival time ( J:199091 )

• mutants succumb to tumors rapidly, dying between P75 and P90

neoplasm

increased salivary gland tumor incidence ( J:199091 )

• rapidly develop aggressive tumors in the salivary glands

• tumors contain transplantable and hyperproliferative tumor propagating cells (CD24+CD29+)

• treatment of cultured CD24+CD29+ tumor cells with the canonical Wnt inhibitor ICG-001 blocks proliferation of these cells

• CD24+CD29+ tumor propagating cells from salivary gland tumors exhibit unrestricted self-renewal in salisphere culture

increased squamous cell carcinoma incidence ( J:199091 )

• tumors arise from the submandibular salivary glands and are classified as salivary gland squamous cell carcinoma

digestive/alimentary system

increased salivary gland tumor incidence ( J:199091 )

• rapidly develop aggressive tumors in the salivary glands

• tumors contain transplantable and hyperproliferative tumor propagating cells (CD24+CD29+)

• treatment of cultured CD24+CD29+ tumor cells with the canonical Wnt inhibitor ICG-001 blocks proliferation of these cells

• CD24+CD29+ tumor propagating cells from salivary gland tumors exhibit unrestricted self-renewal in salisphere culture

endocrine/exocrine glands

increased salivary gland tumor incidence ( J:199091 )

• rapidly develop aggressive tumors in the salivary glands

• tumors contain transplantable and hyperproliferative tumor propagating cells (CD24+CD29+)

• treatment of cultured CD24+CD29+ tumor cells with the canonical Wnt inhibitor ICG-001 blocks proliferation of these cells

• CD24+CD29+ tumor propagating cells from salivary gland tumors exhibit unrestricted self-renewal in salisphere culture

integument

increased hair follicle number ( J:199091 )

• excessive supernumerary hair follicles in the skin

craniofacial

increased salivary gland tumor incidence ( J:199091 )

• rapidly develop aggressive tumors in the salivary glands

• tumors contain transplantable and hyperproliferative tumor propagating cells (CD24+CD29+)

• treatment of cultured CD24+CD29+ tumor cells with the canonical Wnt inhibitor ICG-001 blocks proliferation of these cells

• CD24+CD29+ tumor propagating cells from salivary gland tumors exhibit unrestricted self-renewal in salisphere culture

growth/size/body

increased salivary gland tumor incidence ( J:199091 )

• rapidly develop aggressive tumors in the salivary glands

• tumors contain transplantable and hyperproliferative tumor propagating cells (CD24+CD29+)

• treatment of cultured CD24+CD29+ tumor cells with the canonical Wnt inhibitor ICG-001 blocks proliferation of these cells

• CD24+CD29+ tumor propagating cells from salivary gland tumors exhibit unrestricted self-renewal in salisphere culture

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
salivary gland carcinoma		DOID:0050904		J:199091

Genotype
MGI:5508224

cn13

• Allelic Composition: Ctnnb1^tm1Mmt/Ctnnb1⁺; Krt14^{tm1.1(cre)Wbm}/Krt14⁺
• Genetic Background: involves: 129P2/OlaHsd * 129X1/SvJ

neoplasm

neoplasm ( J:199091 )

N • mice do not develop salivary squamous cell carcinoma

Genotype
MGI:5547811

cn14

• Allelic Composition: Wls^tm1.1Arte/Wls^tm1.1Arte; Krt14^tm1(cre)Wbm/Krt14⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

mortality/aging

premature death ( J:202499 )

• mice die within 10 weeks

integument

epidermal spongiosis ( J:202499 )

abnormal hair growth ( J:202499 )

• hair loss begins during the first hair cycle

sparse hair ( J:202499 )

• less dense at P6

thin hypodermis ( J:202499 )

decreased hair follicle number ( J:202499 )

• fewer follicles develop and degenerate to cyst-like structures

hair follicle degeneration ( J:202499 )

• degenerate to cyst-like structures

thin dermal layer ( J:202499 )

abnormal skin appearance ( J:202499 )

• irritated, flaky and thin skin with exposed blood vessels

• Munro's microabscesses all over the skin

flaky skin ( J:202499 )

reddish skin ( J:202499 )

• red-nose phenotype at P6

scaly skin ( J:202499 )

thin skin ( J:202499 )

abnormal skin physiology ( J:202499 )

• hyperproliferative epidermis with increased proportion of proliferating basal cells but fewer number of proliferating cells in the bulb

increased keratinocyte proliferation ( J:202499 )

impaired skin barrier function ( J:202499 )

• at P6, but not in neonates

skin inflammation ( J:202499 )

• with fluid retention

• neutrophil infiltration in the dermis at P16 that is not reduced by antibiotic treatment

immune system

small thymus medulla ( J:202499 )

• reduced at P90, but not P4 or P28

decreased thymus weight ( J:202499 )

• relative weight at P21 and P65, but not P4

thymus atrophy ( J:202499 )

thymus hypoplasia ( J:202499 )

• at P40, but not P4

abnormal T cell differentiation ( J:202499 )

• T cell maturation is shifted away from alpha/beta T cells in the thymus at P40

increased double-negative T cell number ( J:202499 )

• at P40 in the thymus

decreased double-positive T cell number ( J:202499 )

• at P40 in the thymus

cutaneous mastocytosis ( J:202499 )

• increased mast cell number in the skin

increased neutrophil cell number ( J:202499 )

• neutrophil infiltration in the dermis at P16 that is not reduced by antibiotic treatment

abnormal T cell subpopulation ratio ( J:202499 )

• the ratio of CD4 to CD8 T cells is decreased at P40 in the thymus, lymph node and blood

decreased T cell number ( J:202499 )

• reduced CD3+ T cells in the thymus

decreased gamma-delta T cell number ( J:202499 )

• age-dependent decrease in gamma-delta TCR+ T cells (dendritic epidermal T cells) in the skin

increased macrophage cell number ( J:202499 )

• in the skin

abnormal T cell physiology ( J:202499 )

• dendritic epidermal T cell survival is impaired

increased T cell proliferation ( J:202499 )

• of dendritic epidermal T cell

skin inflammation ( J:202499 )

• with fluid retention

• neutrophil infiltration in the dermis at P16 that is not reduced by antibiotic treatment

vision/eye

abnormal eye morphology ( J:202499 )

• swollen eye

hearing/vestibular/ear

abnormal ear morphology ( J:202499 )

craniofacial

abnormal nose morphology ( J:202499 )

• red-nose phenotype at P6

respiratory system

abnormal nose morphology ( J:202499 )

• red-nose phenotype at P6

adipose tissue

abnormal adipose tissue physiology ( J:202499 )

• mice exhibit lack of fat tissue sustainment

growth/size/body

abnormal nose morphology ( J:202499 )

• red-nose phenotype at P6

decreased body size ( J:202499 )

postnatal growth retardation ( J:202499 )

homeostasis/metabolism

decreased body surface temperature ( J:202499 )

• in adult mice

epidermal spongiosis ( J:202499 )

impaired skin barrier function ( J:202499 )

• at P6, but not in neonates

hematopoietic system

small thymus medulla ( J:202499 )

• reduced at P90, but not P4 or P28

decreased thymus weight ( J:202499 )

• relative weight at P21 and P65, but not P4

thymus atrophy ( J:202499 )

thymus hypoplasia ( J:202499 )

• at P40, but not P4

abnormal T cell differentiation ( J:202499 )

• T cell maturation is shifted away from alpha/beta T cells in the thymus at P40

increased double-negative T cell number ( J:202499 )

• at P40 in the thymus

cutaneous mastocytosis ( J:202499 )

• increased mast cell number in the skin

increased neutrophil cell number ( J:202499 )

• neutrophil infiltration in the dermis at P16 that is not reduced by antibiotic treatment

abnormal T cell subpopulation ratio ( J:202499 )

• the ratio of CD4 to CD8 T cells is decreased at P40 in the thymus, lymph node and blood

decreased T cell number ( J:202499 )

• reduced CD3+ T cells in the thymus

decreased double-positive T cell number ( J:202499 )

• at P40 in the thymus

decreased gamma-delta T cell number ( J:202499 )

• age-dependent decrease in gamma-delta TCR+ T cells (dendritic epidermal T cells) in the skin

increased macrophage cell number ( J:202499 )

• in the skin

abnormal T cell physiology ( J:202499 )

• dendritic epidermal T cell survival is impaired

increased T cell proliferation ( J:202499 )

• of dendritic epidermal T cell

cellular

increased T cell proliferation ( J:202499 )

• of dendritic epidermal T cell

increased keratinocyte proliferation ( J:202499 )

endocrine/exocrine glands

small thymus medulla ( J:202499 )

• reduced at P90, but not P4 or P28

decreased thymus weight ( J:202499 )

• relative weight at P21 and P65, but not P4

thymus atrophy ( J:202499 )

thymus hypoplasia ( J:202499 )

• at P40, but not P4

Genotype
MGI:2673246

cn15

• Allelic Composition: Ctnnb1^tm4Wbm/Ctnnb1^tm4Wbm; Krt14^tm1(cre)Wbm/Krt14⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

integument

abnormal hair growth ( J:69463 )

alopecia ( J:69463 )

• hairless patches at 8 days of age

• hair placodes absent where Catnb is not expressed

• initial phase hair growth occurs until 16 days

• reduced number of zigzag hairs

• hair lost around 4 weeks of age and no regrowth

Genotype
MGI:2673250

cn16

• Allelic Composition: Ctnnb1^tm4Wbm/Ctnnb1^tm4Wbm; Krt14^{tm1.1(cre)Wbm}/Krt14⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

integument

abnormal hair growth ( J:69463 )

alopecia ( J:69463 )

• no hairless skin patches at 8 days of age

• initial phase hair growth occurs until 16 days of age

• reduced number of zigzag hairs

• hair loss around 4 weeks of age and no regrowth

• hair shafts become separated from dermal papillae

Genotype
MGI:6196149

cn17

• Allelic Composition: Krt14^{tm1.1(cre)Wbm}/Krt14⁺; Tg(KRT14-Snai1)1Efu/0; Trp53^tm1Brn/Trp53^tm1Brn
• Genetic Background: involves: 129P2/OlaHsd * CD-1

endocrine/exocrine glands

increased sebaceous gland tumor incidence ( J:229072 )

• sebaceous gland carcinoma

integument

increased sebaceous gland tumor incidence ( J:229072 )

• sebaceous gland carcinoma

increased skin tumor incidence ( J:229072 )

• mice develop skin tumors more rapidly than single Tg(KRT14-Snai1)1Efu expressing mice, with a median latency of 176 days

• however, mice do not develop more tumors than Tg(KRT14-Snai1)1Efu mice alone

• tumors include basal cell carcinoma, squamous cell carcinoma, and sebaceous gland carcinoma and more aggressive carcinosarcomas characterized by the biphasic appearance of intermixed epithelial and mesenchymal elements

increased basal cell carcinoma incidence ( J:229072 )

increased skin squamous cell carcinoma incidence ( J:229072 )

neoplasm

increased sebaceous gland tumor incidence ( J:229072 )

• sebaceous gland carcinoma

increased skin tumor incidence ( J:229072 )

• mice develop skin tumors more rapidly than single Tg(KRT14-Snai1)1Efu expressing mice, with a median latency of 176 days

• however, mice do not develop more tumors than Tg(KRT14-Snai1)1Efu mice alone

• tumors include basal cell carcinoma, squamous cell carcinoma, and sebaceous gland carcinoma and more aggressive carcinosarcomas characterized by the biphasic appearance of intermixed epithelial and mesenchymal elements

increased basal cell carcinoma incidence ( J:229072 )

increased skin squamous cell carcinoma incidence ( J:229072 )

Genotype
MGI:3836769

cn18

• Allelic Composition: Itga3^tm1Son/Itga3^tm1Son; Krt14^tm1(cre)Wbm/Krt14⁺
• Genetic Background: involves: 129P2/OlaHsd * FVB/N

homeostasis/metabolism

enhanced wound healing ( J:145988 )

• wound healing of the epidermis is accelerated

• about 90% of experimental wounds are closed after one week compared to about 60% in controls

• this enhanced wound healing is due to accelerated keratinocyte migration from sides of wound and not from increased proliferation

immune system

skin inflammation ( J:145988 )

• inflammation occurs frequently around 3 to 4 months of age at the ears and around the eyes

integument

skin inflammation ( J:145988 )

• inflammation occurs frequently around 3 to 4 months of age at the ears and around the eyes

alopecia ( J:145988 )

• alopecia starts at 3- to 4- months after birth and progresses with age

blistering ( J:145988 )

• microblisters occur at the dermis-epidermis junction

thick skin ( J:145988 )

• epidermis is thickened around the ears, the eyes, and at sites of microblistering

Genotype
MGI:3812200

cn19

• Allelic Composition: Krt14^tm1Der/Krt14⁺; Tg(KRT14-cre/PGR)1Der/?
• Genetic Background: involves: 129X1/SvJ * FVB * ICR

integument

blistering ( J:67320 )

• after application of a topical antiprogestin, RU486, to the forelimbs and chest of newborn pups so that the cre transgene translocates from the cytoplasm to the nucleus of epidermal cells and becomes active, mice developed blisters filled with fluid on the front legs and paws

• blistering occurs within the basal layer of the epidermis

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
epidermolysis bullosa simplex Dowling-Meara type		DOID:0060735	OMIM:131760	J:67320

Genotype
MGI:3812201

cn20

• Allelic Composition: Krt14^tm1Der/Krt14⁺; Tg(KRT5-cre/PGR)1Der/?
• Genetic Background: involves: 129X1/SvJ * FVB * ICR

integument

blistering ( J:67320 )

• after application of a topical antiprogestin, RU486, to the forelimbs and chest of newborn pups so that the cre transgene translocates from the cytoplasm to the nucleus of epidermal cells and becomes active, mice developed blisters filled with fluid on the front legs and paws

• blistering occurs within the basal layer of the epidermis

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
epidermolysis bullosa simplex Dowling-Meara type		DOID:0060735	OMIM:131760	J:67320