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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID 		Tg(KRT5-rtTA)#Glk
transgene insertion, Adam Glick
MGI:4867436
Summary 10 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
 		Ctnnb1tm2Kem/Ctnnb1tm2Kem
Tg(KRT5-rtTA)#Glk/0
Tg(tetO-cre)1Jaw/0 		involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N MGI:5538307
cn2
 		Tg(KRT5-rtTA)#Glk/0
Tg(tetO-cre)1Jaw/0
Wlstm1.1Lan/Wlstm1.1Lan 		involves: 129S6/SvEvTac * C57BL/6 * FVB/N MGI:5538309
cn3
 		Tg(KRT5-rtTA)#Glk/0
Tg(tetO-cre)1Jaw/0
Wnt10atm1Smr/Wnt10atm1Smr 		involves: 129X1/SvJ * C57BL/6 * FVB/N MGI:5905988
cn4
 		Tg(KRT5-rtTA)#Glk/0
Tg(tetO-Dkk1)1Smr/0 		involves: C57BL/6 * FVB/N * SJL MGI:5538319
cn5
 		Tg(KRT14-Kremen1)1Smr/0
Tg(KRT5-rtTA)#Glk/0
Tg(tetO-Dkk1)1Smr/0 		involves: C57BL/6 * FVB/N * SJL MGI:5538320
cx6
 		Col1a1tm1(tetO-CDKN2A)Ibp/Col1a1+
Tg(KRT5-rtTA)#Glk/0 		involves: 129S4/SvJae * C57BL/6 * FVB MGI:5502570
cx7
 		Col1a1tm1(tetO-CDKN2A)Ibp/Col1a1tm2(tetO-GFP/RNAi:Trp53)Slowe
Tg(KRT5-rtTA)#Glk/0 		involves: 129S4/SvJae * C57BL/6 * FVB MGI:5502571
cx8
 		Tg(KRT5-rtTA)#Glk/0
Tg(tetO-Mir31)#Zhyu/0 		involves: C57BL/6J * FVB/N MGI:6358362
cx9
 		Tg(KRT5-rtTA)#Glk/0
Tg(tetO/CMV-Dek,-luc)317Siwe/0 		involves: FVB/N MGI:6241411
cx10
 		Tg(KRT5-rtTA)#Glk/0
Tg(tetO-S100a7a)#Yus/0 		involves: FVB/N MGI:4936856


Genotype
MGI:5538307
cn1
Allelic
Composition		 Ctnnb1tm2Kem/Ctnnb1tm2Kem
Tg(KRT5-rtTA)#Glk/0
Tg(tetO-cre)1Jaw/0
Genetic
Background		 involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm2Kem mutation (1 available); any Ctnnb1 mutation (49 available)
Tg(KRT5-rtTA)#Glk mutation (0 available)
Tg(tetO-cre)1Jaw mutation (6 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
integument
increased hair follicle apoptosis ( J:204142 )
• with doxycycline induction from P8, hair follicles contain numerous apoptotic cells (more than in mutants with transgenic expression of Dkk1, or Dkk1 and Kremen
abnormal hair growth ( J:204142 )
• with doxycline induction from P30, mutants completely lack external hair when examined at P100-102
abnormal hair follicle morphology ( J:204142 )
• with doxycycline induction from P8 hair follicles in mutants display structural defects at P24, including widened infundibulum and loss of a clearly distinguishable secondary hair germ
abnormal hair follicle infundibulum morphology ( J:204142 )
• with doxycycline induction from P8 hair follicles display a widened infundibulum at P24
decreased hair follicle number ( J:204142 )
• with doxycycline induction from P30, hair follicles are mainly absent in mutants
hair follicle degeneration ( J:204142 )
• with doxycycline induction from P30, hair follicles degrade and form utricles by P180
abnormal hair cycle anagen phase ( J:204142 )
• when doxycline induction is performed at P4 or P7 and dorsal skin harvested at P8 or P14, hair follicles in treated skin show cessation of anagen
• with doxycycline induction from P50 and hair plucking at P54, proliferation of secondary hair germ cells of follicles is decreased or absent and a new hair growth phase is not observed by P57
• with induction from P17 (catagen phase), follicles fail to enter anagen
accelerated hair follicle regression ( J:204142 )
• when doxycline induction is performed at P4 or P7 and dorsal skin harvested at P8 or P14, hair follicles in treated skin show entry into a premature regression phase compared to controls
abnormal dermis papillary layer morphology ( J:204142 )
• dermal papillary cells are observed 'stranded' in the epidermis or at the end of 'streamers' of degenerating hair follicles
abnormal epidermal layer morphology ( J:204142 )
• when doxycline induction is performed from P4 to P60, enlargement of intercellular spaces and some cell membrane protrusions are observed in some areas of mutant skins
thick epidermis stratum basale ( J:204142 )
• when doxycline induction is performed from P4 to P60, expansion of the basal layer is observed
thick epidermis suprabasal layer ( J:204142 )
• when doxycline induction is performed from P4 to P60, expansion of the suprabasal layer is observed
abnormal keratinocyte morphology ( J:204142 )
• when doxycline induction is performed from P4 to P60, some keratinocytes display long membranous protrusions
thick epidermis ( J:204142 )
• when doxycline induction is performed from P4 to P60, epidermis displays thickening and hyperproliferation
• with doxycycline induction from P30, epidermis is thickened at P100

cellular
increased hair follicle apoptosis ( J:204142 )
• with doxycycline induction from P8, hair follicles contain numerous apoptotic cells (more than in mutants with transgenic expression of Dkk1, or Dkk1 and Kremen




Genotype
MGI:5538309
cn2
Allelic
Composition		 Tg(KRT5-rtTA)#Glk/0
Tg(tetO-cre)1Jaw/0
Wlstm1.1Lan/Wlstm1.1Lan
Genetic
Background		 involves: 129S6/SvEvTac * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(KRT5-rtTA)#Glk mutation (0 available)
Tg(tetO-cre)1Jaw mutation (6 available)
Wlstm1.1Lan mutation (1 available); any Wls mutation (38 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
integument
abnormal hair follicle morphology ( J:204142 )
• in P60 animals, hair follicle structures are retained in absence of external hair, but display abnormalities including cyst formation
abnormal hair cycle catagen phase ( J:204142 )
• cre induction at P4 causes hair follicle regression by P14 without loss of bulge stem cell markers
abnormal epidermal layer morphology ( J:204142 )
• when doxycline induction is performed from P4 to P18, epidermis exhibits increased proliferation as well as expanded expression of basal and suprabasal markers and hyperproliferation markers
• when doxycline induction is performed from P4 to P18, enlargement of intercellular spaces and some cell membrane protrusions are observed in some areas of mutant skins at P60
• defects of the interfollicular epidermis similar to those observed in conditional Ctnnb1 mutants are seen in induced mutants

immune system
cutaneous mastocytosis ( J:204142 )
• with doxycycline induction from P4-P18, mast cell number in the dermis is increased at P60

hematopoietic system
cutaneous mastocytosis ( J:204142 )
• with doxycycline induction from P4-P18, mast cell number in the dermis is increased at P60




Genotype
MGI:5905988
cn3
Allelic
Composition		 Tg(KRT5-rtTA)#Glk/0
Tg(tetO-cre)1Jaw/0
Wnt10atm1Smr/Wnt10atm1Smr
Genetic
Background		 involves: 129X1/SvJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(KRT5-rtTA)#Glk mutation (0 available)
Tg(tetO-cre)1Jaw mutation (6 available)
Wnt10atm1Smr mutation (0 available); any Wnt10a mutation (19 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
integument
enlarged sebaceous gland ( J:242196 )
• when treated with doxycycline at P25
abnormal sweat gland morphology ( J:242196 )
• fail to extend when treated with doxycycline in early postnatal life
• regression of sweat glands when treated with doxycycline at P20
abnormal sebaceous lipid secretion ( J:242196 )
• elevated lipid production when treated with doxycycline at P25
hypohidrosis ( J:242196 )
• when treated with doxycycline at P20
small hair follicles ( J:242196 )
• minitaturized when treated with doxycycline at P25
abnormal hair cycle anagen phase ( J:242196 )
• delayed initiation of anagen until P29, when treated with doxycycline at P18
accelerated hair follicle regression ( J:242196 )
• premature when treated with doxycycline at P9
• however, hair follicle regression isnt observed when treated with doxycycline at P25
abnormal hair follicle physiology ( J:242196 )
• slightly reduced proliferation when treated with doxycycline at P25

craniofacial
abnormal tongue morphology ( J:242196 )
• flattened surface when treated with doxycycline in early postnatal life
abnormal filiform papillae morphology ( J:242196 )
• progressive from P7 when treated with doxycycline in early postnatal life
abnormal fungiform papillae morphology ( J:242196 )
• progressive from P7 when treated with doxycycline in early postnatal life
abnormal gustatory papilla taste bud morphology ( J:242196 )
• miniaturized when treated with doxycycline in early postnatal life
• decreased taste bud in fungiform and circumvallate papillae when treated with doxycycline in early postnatal life

cellular
decreased cell proliferation ( J:242196 )
• decreased basal cell proliferation in the filiform papillae and plantar epithelium, fungiform and circumvallate taste buds and sweat buds when treated with doxycycline at in either the early postnatal period, or in adult life

taste/olfaction
abnormal gustatory papilla taste bud morphology ( J:242196 )
• miniaturized when treated with doxycycline in early postnatal life
• decreased taste bud in fungiform and circumvallate papillae when treated with doxycycline in early postnatal life

digestive/alimentary system
abnormal tongue morphology ( J:242196 )
• flattened surface when treated with doxycycline in early postnatal life
abnormal filiform papillae morphology ( J:242196 )
• progressive from P7 when treated with doxycycline in early postnatal life
abnormal fungiform papillae morphology ( J:242196 )
• progressive from P7 when treated with doxycycline in early postnatal life
abnormal gustatory papilla taste bud morphology ( J:242196 )
• miniaturized when treated with doxycycline in early postnatal life
• decreased taste bud in fungiform and circumvallate papillae when treated with doxycycline in early postnatal life

endocrine/exocrine glands
enlarged sebaceous gland ( J:242196 )
• when treated with doxycycline at P25
abnormal sweat gland morphology ( J:242196 )
• fail to extend when treated with doxycycline in early postnatal life
• regression of sweat glands when treated with doxycycline at P20
abnormal sebaceous lipid secretion ( J:242196 )
• elevated lipid production when treated with doxycycline at P25
hypohidrosis ( J:242196 )
• when treated with doxycycline at P20

growth/size/body
abnormal tongue morphology ( J:242196 )
• flattened surface when treated with doxycycline in early postnatal life
abnormal filiform papillae morphology ( J:242196 )
• progressive from P7 when treated with doxycycline in early postnatal life
abnormal fungiform papillae morphology ( J:242196 )
• progressive from P7 when treated with doxycycline in early postnatal life
abnormal gustatory papilla taste bud morphology ( J:242196 )
• miniaturized when treated with doxycycline in early postnatal life
• decreased taste bud in fungiform and circumvallate papillae when treated with doxycycline in early postnatal life




Genotype
MGI:5538319
cn4
Allelic
Composition		 Tg(KRT5-rtTA)#Glk/0
Tg(tetO-Dkk1)1Smr/0
Genetic
Background		 involves: C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
integument
abnormal hair growth ( J:204142 )
• with doxycycline induction starting at P1, mutants completely lack external hair when examined at P100-102
abnormal hair follicle morphology ( J:204142 )
• induction at P4 of P7, reduced proliferation is observed in mutant follicles at P8 or P14
• with doxycycline induction starting at P1, mutant hair follicles show some structural abnormalities by P185
• with doxycycline induction from P4, follicles have slightly increased numbers of apoptotic cells
• with doxycycline treatment starting at P1, no follicle proliferation or hair shaft differentiation is observed; with withdrawal of dox at P100, these are restored
abnormal hair cycle anagen phase ( J:204142 )
• when doxycline induction is performed at P4 or P7 and dorsal skin harvested at P8 or P14, hair follicles in treated skin show cessation of anagen
• with doxycycline treatment starting at P1, hair follicles are arrested in very early anagen; withdrawal of dox at P100 results in follicles spontaneously progressing to full anagen in 15 days
• with induction from P17 (catagen phase), follicles are arrested in early anagen at P30
• with doxycycline induction from P50 and hair plucking at P54, by P57 mutant hair follicles fail to progress through anagen
accelerated hair follicle regression ( J:204142 )
• when doxycline induction is performed at P4 or P7 and dorsal skin harvested at P8 or P14, hair follicles in treated skin show entry into a premature regression phase compared to controls




Genotype
MGI:5538320
cn5
Allelic
Composition		 Tg(KRT14-Kremen1)1Smr/0
Tg(KRT5-rtTA)#Glk/0
Tg(tetO-Dkk1)1Smr/0
Genetic
Background		 involves: C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cellular
increased hair follicle apoptosis ( J:204142 )
• with doxycycline induction from P4, follicles have slightly increased numbers of apoptotic cells

integument
increased hair follicle apoptosis ( J:204142 )
• with doxycycline induction from P4, follicles have slightly increased numbers of apoptotic cells
abnormal hair growth ( J:204142 )
• with doxycline induction from P30, mutants have completely lost external hair by P103
abnormal hair cycle anagen phase ( J:204142 )
• when doxycline induction is performed at P4 or P7 and dorsal skin harvested at P8 or P14, hair follicles in treated skin show cessation of anagen; effect is enhanced in triple mutants compared to double mutants by coexpression of Dkk1 with Kremen1
• with induction from P17 (catagen phase), follicles are arrested in early anagen at earlier time than double mutants expressing Dkk1 alone
accelerated hair follicle regression ( J:204142 )
• when doxycline induction is performed at P4 or P7 and dorsal skin harvested at P8 or P14, hair follicles in treated skin show entry into a premature regression phase compared to controls; effect is enhanced in triple mutants compared to double mutants by coexpression of Dkk1 with Kremen1




Genotype
MGI:5502570
cx6
Allelic
Composition		 Col1a1tm1(tetO-CDKN2A)Ibp/Col1a1+
Tg(KRT5-rtTA)#Glk/0
Genetic
Background		 involves: 129S4/SvJae * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-CDKN2A)Ibp mutation (0 available); any Col1a1 mutation (163 available)
Tg(KRT5-rtTA)#Glk mutation (0 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
integument
abnormal hair follicle development ( J:196969 )
• dysfunctional hair follicle stem cells in doxycycline-treated mice due to blockage of proliferation
decreased hair follicle number ( J:196969 )
• noticeable after 10 days and pronounced by 6 weeks in doxycycline-treated mice
abnormal hair cycle ( J:196969 )
• bulge stem cells in doxycycline-treated mice fail to enter into the cell cycle and initiate anagen with follicles remaining in a telogen-like state unlike in control mice
• resilencing in doxycycline re-treated mice prevents hair follicle growth unlike in control mice
• however, withdrawal of doxycycline restores entry into anagen
thick epidermis ( J:196969 )
• in some doxycycline-treated mice
abnormal skin physiology ( J:196969 )
• after 2 days, doxycycline-treated mice exhibit decreased proliferation and increased apoptosis of basal epidermal cells compared with control mice
• after 1 week, mice exhibit hyperproliferation of basal cells that decreases after longer induction times and increased cellular replicative senescence compared with control mice
• however, apoptosis rates are normal after 1 week of induction and removal of doxycycline prevents further increases in senescence

cellular
early cellular replicative senescence ( J:196969 )
• after 1 week, doxycycline-treated mice exhibit increased cellular senescence in the epidermis compared with control mice
• however, removal of doxycycline prevents further increases in senescence and treatment with TPA does not increase senescence




Genotype
MGI:5502571
cx7
Allelic
Composition		 Col1a1tm1(tetO-CDKN2A)Ibp/Col1a1tm2(tetO-GFP/RNAi:Trp53)Slowe
Tg(KRT5-rtTA)#Glk/0
Genetic
Background		 involves: 129S4/SvJae * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm1(tetO-CDKN2A)Ibp mutation (0 available); any Col1a1 mutation (163 available)
Col1a1tm2(tetO-GFP/RNAi:Trp53)Slowe mutation (0 available); any Col1a1 mutation (163 available)
Tg(KRT5-rtTA)#Glk mutation (0 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
integument
integument phenotype ( J:196969 )
N
• doxycycline-treated mice exhibit normal cellular senescence in the epidermis

cellular
cellular phenotype ( J:196969 )
N
• doxycycline-treated mice exhibit normal cellular senescence in the epidermis




Genotype
MGI:6358362
cx8
Allelic
Composition		 Tg(KRT5-rtTA)#Glk/0
Tg(tetO-Mir31)#Zhyu/0
Genetic
Background		 involves: C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
behavior/neurological
abnormal nursing ( J:271420 )
• doxycyline(dox)-treated females are incapable of nursing their pups, leading to neonatal lethality

endocrine/exocrine glands
increased mammary gland epithelial cell proliferation ( J:271420 )
• dox-treated mammary glands exhibit an increase in mammary epithelial cell proliferation
abnormal mammary gland morphology ( J:271420 )
• beta-casein is completely absent in dox-treated glands
abnormal mammary gland development ( J:271420 )
• dox-treated mice show mammary stem cell expansion at the expense of differentiation, showing a 4-fold larger population of Lin-CD24+CD29high cells
• marker analysis of dox-treated mice indicates that differentiation of mammary epithelial cells is inhibited
• in vitro colony formation assay with purified CD24+CD29high cells from dox-treated mice shows that the number of primary colonies that form is similar to controls but the numbers of secondary, tertiary, and subsequent colonies are increased indicating increased mammary stem cell self-renewal
• basal progenitor cells from dox-treated mice grown on feeder cell layers show an increase in the number of solid basal colonies at the cost of acinar colonies indicating an inhibition of luminal differentiation or suppression of luminal cell colony formation
abnormal mammary gland growth during pregnancy ( J:271420 )
• dox-treated mammary glands fail to form alveoli and retain undifferentiated ductal structures at post-pregnancy 14.5 and lactation day 1
abnormal mammary gland epithelium morphology ( J:271420 )
• marker analysis of dox-treated mice indicates that differentiation of mammary epithelial cells is inhibited
abnormal mammary gland duct morphology ( J:271420 )
• dox-treated mammary glands fail to form alveoli and retain undifferentiated ductal structures at post-pregnancy 14.5 and lactation day 1
abnormal branching of the mammary ductal tree ( J:271420 )
• dox-treated mice show mildly inhibited mammary branching and ductal elongation at 6 weeks of age, however by 10 weeks of age, these effects are no longer seen
• mammary glands of all dox-treated 12 week old mice show no tertiary branch development and varying defects in ductal elongation and branching, and the appearance of multiple terminal end bud-like structures
mammary gland duct hyperplasia ( J:271420 )
• dox-treated mice have thicker mammary ducts, characterized by an increase in cell layers, at 12 weeks of age
abnormal mammary gland alveolus morphology ( J:271420 )
• dox-treated mammary glands fail to form alveoli and retain undifferentiated ductal structures at post-pregnancy 14.5 and lactation day 1

cellular
increased mammary gland epithelial cell proliferation ( J:271420 )
• dox-treated mammary glands exhibit an increase in mammary epithelial cell proliferation

integument
increased mammary gland epithelial cell proliferation ( J:271420 )
• dox-treated mammary glands exhibit an increase in mammary epithelial cell proliferation
abnormal mammary gland morphology ( J:271420 )
• beta-casein is completely absent in dox-treated glands
abnormal mammary gland development ( J:271420 )
• dox-treated mice show mammary stem cell expansion at the expense of differentiation, showing a 4-fold larger population of Lin-CD24+CD29high cells
• marker analysis of dox-treated mice indicates that differentiation of mammary epithelial cells is inhibited
• in vitro colony formation assay with purified CD24+CD29high cells from dox-treated mice shows that the number of primary colonies that form is similar to controls but the numbers of secondary, tertiary, and subsequent colonies are increased indicating increased mammary stem cell self-renewal
• basal progenitor cells from dox-treated mice grown on feeder cell layers show an increase in the number of solid basal colonies at the cost of acinar colonies indicating an inhibition of luminal differentiation or suppression of luminal cell colony formation
abnormal mammary gland growth during pregnancy ( J:271420 )
• dox-treated mammary glands fail to form alveoli and retain undifferentiated ductal structures at post-pregnancy 14.5 and lactation day 1
abnormal mammary gland epithelium morphology ( J:271420 )
• marker analysis of dox-treated mice indicates that differentiation of mammary epithelial cells is inhibited
abnormal mammary gland duct morphology ( J:271420 )
• dox-treated mammary glands fail to form alveoli and retain undifferentiated ductal structures at post-pregnancy 14.5 and lactation day 1
abnormal branching of the mammary ductal tree ( J:271420 )
• dox-treated mice show mildly inhibited mammary branching and ductal elongation at 6 weeks of age, however by 10 weeks of age, these effects are no longer seen
• mammary glands of all dox-treated 12 week old mice show no tertiary branch development and varying defects in ductal elongation and branching, and the appearance of multiple terminal end bud-like structures
mammary gland duct hyperplasia ( J:271420 )
• dox-treated mice have thicker mammary ducts, characterized by an increase in cell layers, at 12 weeks of age
abnormal mammary gland alveolus morphology ( J:271420 )
• dox-treated mammary glands fail to form alveoli and retain undifferentiated ductal structures at post-pregnancy 14.5 and lactation day 1

reproductive system
abnormal mammary gland growth during pregnancy ( J:271420 )
• dox-treated mammary glands fail to form alveoli and retain undifferentiated ductal structures at post-pregnancy 14.5 and lactation day 1




Genotype
MGI:6241411
cx9
Allelic
Composition		 Tg(KRT5-rtTA)#Glk/0
Tg(tetO/CMV-Dek,-luc)317Siwe/0
Genetic
Background		 involves: FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(KRT5-rtTA)#Glk mutation (0 available)
Tg(tetO/CMV-Dek,-luc)317Siwe mutation (1 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
craniofacial
abnormal tongue squamous epithelium morphology ( J:261249 )
• trend toward increased cellular proliferation in the tongue and esophagus in mice treated with 4NQO, a chemical carcinogen

digestive/alimentary system
abnormal tongue squamous epithelium morphology ( J:261249 )
• trend toward increased cellular proliferation in the tongue and esophagus in mice treated with 4NQO, a chemical carcinogen
esophagus hyperplasia ( J:261249 )
• trend toward increased cellular proliferation in the tongue and esophagus in mice treated with 4NQO, a chemical carcinogen

growth/size/body
abnormal tongue squamous epithelium morphology ( J:261249 )
• trend toward increased cellular proliferation in the tongue and esophagus in mice treated with 4NQO, a chemical carcinogen
esophagus hyperplasia ( J:261249 )
• trend toward increased cellular proliferation in the tongue and esophagus in mice treated with 4NQO, a chemical carcinogen

homeostasis/metabolism
increased incidence of tumors by chemical induction ( J:261249 )
• increased incidence of gross esophageal squamous cell carcinoma with stromal invasion in mice treated with 4NQO, a chemical carcinogen, as compared to 4NQO dox-treated mice

mortality/aging
premature death ( J:261249 )
• survival of mice treated with 4NQO is less than 60% as compared to 4NQO dox-treated mice, which survive to at least 45 weeks

neoplasm
increased incidence of tumors by chemical induction ( J:261249 )
• increased incidence of gross esophageal squamous cell carcinoma with stromal invasion in mice treated with 4NQO, a chemical carcinogen, as compared to 4NQO dox-treated mice
increased squamous cell carcinoma incidence ( J:261249 )
• increased incidence of gross esophageal squamous cell carcinoma with stromal invasion in mice treated with 4NQO, a chemical carcinogen, as compared to 4NQO dox-treated mice
• incidence of oral squamous cell carcinoma is not increased




Genotype
MGI:4936856
cx10
Allelic
Composition		 Tg(KRT5-rtTA)#Glk/0
Tg(tetO-S100a7a)#Yus/0
Genetic
Background		 involves: FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
immune system
abnormal chemokine secretion ( J:168000 )
• TPA-treated mice exhibit a 1.6-fold increase in RANTES (CCL5) production, 3-fold increase in MIP2 (CXCL2) production, and 3.7-fold increase in GM-CSF production compared with similarly treated single transgenic mice
increased interleukin-1 alpha secretion ( J:168000 )
• 3-fold in TPA-treated mice
increased tumor necrosis factor secretion ( J:168000 )
• 2-fold in TPA-treated mice

integument
abnormal skin morphology ( J:168000 )
• mice exhibit increased infiltration of CD3+ and CD4+ T cells in nonlesion skin unlike single transgenic mice
psoriasis ( J:168000 )
• mice treated with TPA or subjected to tape stripping develop psoriasis-like lesions to a greater extent than in similarly treated single transgenic mice

Mouse Models of Human Disease
 DO ID OMIM ID(s) Ref(s)
psoriasis DOID:8893 OMIM:PS177900
 J:168000




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Send questions and comments to User Support. 		last database update
11/19/2024
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