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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Nkx3-1+
wild type
MGI:2153462
Summary 7 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
ht1
Nkx3-1tm1Mms/Nkx3-1+ either: (involves: 129S1/Sv * 129S1/SvImJ) or (involves: 129S1/Sv * 129S1/SvImJ * C57BL/6J) MGI:2175153
ht2
Nkx3-1tm1Hha/Nkx3-1+ involves: 129S4/SvJae * C57BL/6 MGI:2175151
ht3
Nkx3-1tm2Mms/Nkx3-1+ involves: 129S6/SvEvTac * C57BL/6 MGI:3719105
cn4
Braftm1Mmcm/Braftm1Mmcm
Nkx3-1tm4(cre/ERT2)Mms/Nkx3-1+
Ptentm1Hwu/Pten+
involves: 129P2/OlaHsd * 129S4/SvJae * 129S6/SvEvTac * C57BL/6 MGI:5543907
cn5
Nkx3-1tm4(cre/ERT2)Mms/Nkx3-1+
Ptentm1Hwu/Ptentm1Hwu
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 MGI:4365721
cn6
Klf6tm1Fjs/Klf6tm1Fjs
Nkx3-1tm3(cre)Mms/Nkx3-1+
involves: 129/Sv * C57BL/6 MGI:4361338
cx7
Nkx3-1tm1Mms/Nkx3-1+
Ptentm1Rps/Pten+
involves: 129S1/Sv * 129S1/SvImJ * C57BL/6J MGI:5569928


Genotype
MGI:2175153
ht1
Allelic
Composition
Nkx3-1tm1Mms/Nkx3-1+
Genetic
Background
either: (involves: 129S1/Sv * 129S1/SvImJ) or (involves: 129S1/Sv * 129S1/SvImJ * C57BL/6J)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nkx3-1tm1Mms mutation (0 available); any Nkx3-1 mutation (34 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• at 1 year, the anterior prostate of heterozygotes exhibits epithelial hyperplasia of reduced severity relative to homozygotes
• at 1 year, the anterior prostate of heterozygotes exhibits epithelial dysplasia of reduced severity relative to homozygotes
• in addition, heterozygous dorsolateral prostates display a mild dysplasia relative to wild-type
• adult heterozygotes exhibit progressive prostate epithelial hyperplasia of reduced severity relative to homozygotes
• at 6 weeks, heterozygotes exhibit a 4.5-fold increase in epithelial cell proliferation in the anterior prostate relative to wild-type mice
• adult heterozygotes show a significant reduction or loss of major secretory proteins in ventral prostate secretions

reproductive system
• at 1 year, the anterior prostate of heterozygotes exhibits epithelial hyperplasia of reduced severity relative to homozygotes
• at 1 year, the anterior prostate of heterozygotes exhibits epithelial dysplasia of reduced severity relative to homozygotes
• in addition, heterozygous dorsolateral prostates display a mild dysplasia relative to wild-type
• adult heterozygotes exhibit progressive prostate epithelial hyperplasia of reduced severity relative to homozygotes
• at 6 weeks, heterozygotes exhibit a 4.5-fold increase in epithelial cell proliferation in the anterior prostate relative to wild-type mice
• adult heterozygotes show a significant reduction or loss of major secretory proteins in ventral prostate secretions

neoplasm
• at 1 year, the heterozygous anterior prostate shows epithelial hyperplasia and dysplasia along with a marked increase in proliferating cells, modeling a preneoplastic condition




Genotype
MGI:2175151
ht2
Allelic
Composition
Nkx3-1tm1Hha/Nkx3-1+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nkx3-1tm1Hha mutation (0 available); any Nkx3-1 mutation (34 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• at 10 months, heterozygotes exhibit dysplastic changes in the anterior prostate, although of reduced severity relative to homozygotes
• at 2 months, heterozygotes exhibit a normal ductal epithelium in the anterior prostate (AP) relative to wild-type mice; however, moderate AP hyperplasia is observed at 10 months
• by 10 months, heterozygotes also exhibit epithelial hyperplasia in the dorsolateral prostate, although of reduced severity relative to homozygotes
• similar to homozygotes, no hyperplasia is observed in heterozygous ventral prostatic lobes

endocrine/exocrine glands
• at 10 months, heterozygotes exhibit dysplastic changes in the anterior prostate, although of reduced severity relative to homozygotes
• at 2 months, heterozygotes exhibit a normal ductal epithelium in the anterior prostate (AP) relative to wild-type mice; however, moderate AP hyperplasia is observed at 10 months
• by 10 months, heterozygotes also exhibit epithelial hyperplasia in the dorsolateral prostate, although of reduced severity relative to homozygotes
• similar to homozygotes, no hyperplasia is observed in heterozygous ventral prostatic lobes




Genotype
MGI:3719105
ht3
Allelic
Composition
Nkx3-1tm2Mms/Nkx3-1+
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nkx3-1tm2Mms mutation (1 available); any Nkx3-1 mutation (34 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
N
• prostate budding is normal




Genotype
MGI:5543907
cn4
Allelic
Composition
Braftm1Mmcm/Braftm1Mmcm
Nkx3-1tm4(cre/ERT2)Mms/Nkx3-1+
Ptentm1Hwu/Pten+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129S6/SvEvTac * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (4 available); any Braf mutation (62 available)
Nkx3-1tm4(cre/ERT2)Mms mutation (13 available); any Nkx3-1 mutation (34 available)
Ptentm1Hwu mutation (17 available); any Pten mutation (86 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants develop lethal prostate cancer 4 months after tamoxifen induction

neoplasm
• mutants develop lethal prostate cancer 4 months after tamoxifen induction
• tumors are large and highly proliferative and are primarily composed of luminal epithelial cells
• tamoxifen treated mutants do not display significant tumor regression at 2 weeks following castration, indicating that tumors are resistant to castration
• tumors from tamoxifen treated mutants show absence of cellular senescence and are highly proliferative
• treatment of tamoxifen treated mutants with a combination of rapamycin and PD0325901 (a mitogen-activated protein/extracellular signal-regulated kinase inhibitor) results in a reduction in tumor weight, growth, and proliferation
• tamoxifen treated mutants develop invasive adenocarcinoma by 2-3 months after tamoxifen induction
• tamoxifen treated mutants display prostate intraepithelial neoplasia (PIN) by 2-4 weeks after tamoxifen induction
• metastases to lungs and lymph nodes are seen in tamoxifen treated mutants and disseminated tumor cells are seen in the bone marrow

endocrine/exocrine glands
• mutants develop lethal prostate cancer 4 months after tamoxifen induction
• tumors are large and highly proliferative and are primarily composed of luminal epithelial cells
• tamoxifen treated mutants do not display significant tumor regression at 2 weeks following castration, indicating that tumors are resistant to castration
• tumors from tamoxifen treated mutants show absence of cellular senescence and are highly proliferative
• treatment of tamoxifen treated mutants with a combination of rapamycin and PD0325901 (a mitogen-activated protein/extracellular signal-regulated kinase inhibitor) results in a reduction in tumor weight, growth, and proliferation
• tamoxifen treated mutants develop invasive adenocarcinoma by 2-3 months after tamoxifen induction
• tamoxifen treated mutants display prostate intraepithelial neoplasia (PIN) by 2-4 weeks after tamoxifen induction

reproductive system
• mutants develop lethal prostate cancer 4 months after tamoxifen induction
• tumors are large and highly proliferative and are primarily composed of luminal epithelial cells
• tamoxifen treated mutants do not display significant tumor regression at 2 weeks following castration, indicating that tumors are resistant to castration
• tumors from tamoxifen treated mutants show absence of cellular senescence and are highly proliferative
• treatment of tamoxifen treated mutants with a combination of rapamycin and PD0325901 (a mitogen-activated protein/extracellular signal-regulated kinase inhibitor) results in a reduction in tumor weight, growth, and proliferation
• tamoxifen treated mutants develop invasive adenocarcinoma by 2-3 months after tamoxifen induction
• tamoxifen treated mutants display prostate intraepithelial neoplasia (PIN) by 2-4 weeks after tamoxifen induction




Genotype
MGI:4365721
cn5
Allelic
Composition
Nkx3-1tm4(cre/ERT2)Mms/Nkx3-1+
Ptentm1Hwu/Ptentm1Hwu
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nkx3-1tm4(cre/ERT2)Mms mutation (13 available); any Nkx3-1 mutation (34 available)
Ptentm1Hwu mutation (17 available); any Pten mutation (86 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• castrated male mice show rapid formation of high-grade PIN and carcinoma after androgen-mediated prostate regeneration with evidence of microinvasion
• castrated male mice show rapid formation of high-grade PIN and carcinoma after androgen-mediated prostate regeneration with evidence of microinvasion (J:153425)
• mutants show extensive prostate intraepithelial neoplasia (PIN) III and PIN IV 9-12 months after tamoxifen induction, with some areas of squamous papilloma, however mutants rarely develop lethal prostate cancer up to 2 years following tamoxifen induction (J:191327)

reproductive system
• castrated male mice show rapid formation of high-grade PIN and carcinoma after androgen-mediated prostate regeneration with evidence of microinvasion
• castrated male mice show rapid formation of high-grade PIN and carcinoma after androgen-mediated prostate regeneration with evidence of microinvasion (J:153425)
• mutants show extensive prostate intraepithelial neoplasia (PIN) III and PIN IV 9-12 months after tamoxifen induction, with some areas of squamous papilloma, however mutants rarely develop lethal prostate cancer up to 2 years following tamoxifen induction (J:191327)

endocrine/exocrine glands
• castrated male mice show rapid formation of high-grade PIN and carcinoma after androgen-mediated prostate regeneration with evidence of microinvasion
• castrated male mice show rapid formation of high-grade PIN and carcinoma after androgen-mediated prostate regeneration with evidence of microinvasion (J:153425)
• mutants show extensive prostate intraepithelial neoplasia (PIN) III and PIN IV 9-12 months after tamoxifen induction, with some areas of squamous papilloma, however mutants rarely develop lethal prostate cancer up to 2 years following tamoxifen induction (J:191327)




Genotype
MGI:4361338
cn6
Allelic
Composition
Klf6tm1Fjs/Klf6tm1Fjs
Nkx3-1tm3(cre)Mms/Nkx3-1+
Genetic
Background
involves: 129/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Klf6tm1Fjs mutation (0 available); any Klf6 mutation (15 available)
Nkx3-1tm3(cre)Mms mutation (0 available); any Nkx3-1 mutation (34 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Abnormality in ductal branching in the Klf6tm1Fjs/Klf6tm1Fjs Nkx3-1tm3(cre)Mms/Nkx3-1+ prostate epithelium

endocrine/exocrine glands
• lacks secondary branches
• epithelial infolding is significantly reduced resulting in a defined layer of epithelial cells outlining the main ducts
• impaired branching is seen in the anterior prostate in all males by P5
• at 6 months and 1 year of age most mature prostates still lack secondary branching in the anterior prostate
• branching defects are not as apparent in the dorsal and ventral prostates possibly as a result of less efficient Cre mediated recombination
• in the dorsal and ventral prostates the luminal spaces of the ducts are increased
• in the anterior prostate, epithelial infolding is significantly reduced resulting in a defined layer of epithelial cells outlining the main ducts

reproductive system
• lacks secondary branches
• epithelial infolding is significantly reduced resulting in a defined layer of epithelial cells outlining the main ducts
• impaired branching is seen in the anterior prostate in all males by P5
• at 6 months and 1 year of age most mature prostates still lack secondary branching in the anterior prostate
• branching defects are not as apparent in the dorsal and ventral prostates possibly as a result of less efficient Cre mediated recombination
• in the dorsal and ventral prostates the luminal spaces of the ducts are increased
• in the anterior prostate, epithelial infolding is significantly reduced resulting in a defined layer of epithelial cells outlining the main ducts




Genotype
MGI:5569928
cx7
Allelic
Composition
Nkx3-1tm1Mms/Nkx3-1+
Ptentm1Rps/Pten+
Genetic
Background
involves: 129S1/Sv * 129S1/SvImJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nkx3-1tm1Mms mutation (0 available); any Nkx3-1 mutation (34 available)
Ptentm1Rps mutation (0 available); any Pten mutation (86 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• early carcinoma lesions are seen in the prostate at 6 months of age
• at 6 months of age, high-grade prostatic intraepithelial neoplasia/early carcinoma lesions are seen in 36% of prostates, and by 12 months, all mice show lesions
• multifocal lesions in the prostate are comprised of poorly differentiated cells with prominent and multiple nucleoli, an increased nuclear/cytoplasmic ratio, and frequent mitotic figures
• lesions usually fill the affected prostatic ducts and are highly vascularized, show an increase in cytokeratins, an absence of basal epithelium, and a high proliferative index
• lesions show absence of Nkx3-1 protein expression, although mRNA is present and allelic loss of Pten

endocrine/exocrine glands
• early carcinoma lesions are seen in the prostate at 6 months of age
• at 6 months of age, high-grade prostatic intraepithelial neoplasia/early carcinoma lesions are seen in 36% of prostates, and by 12 months, all mice show lesions
• multifocal lesions in the prostate are comprised of poorly differentiated cells with prominent and multiple nucleoli, an increased nuclear/cytoplasmic ratio, and frequent mitotic figures
• lesions usually fill the affected prostatic ducts and are highly vascularized, show an increase in cytokeratins, an absence of basal epithelium, and a high proliferative index
• lesions show absence of Nkx3-1 protein expression, although mRNA is present and allelic loss of Pten

reproductive system
• early carcinoma lesions are seen in the prostate at 6 months of age
• at 6 months of age, high-grade prostatic intraepithelial neoplasia/early carcinoma lesions are seen in 36% of prostates, and by 12 months, all mice show lesions
• multifocal lesions in the prostate are comprised of poorly differentiated cells with prominent and multiple nucleoli, an increased nuclear/cytoplasmic ratio, and frequent mitotic figures
• lesions usually fill the affected prostatic ducts and are highly vascularized, show an increase in cytokeratins, an absence of basal epithelium, and a high proliferative index
• lesions show absence of Nkx3-1 protein expression, although mRNA is present and allelic loss of Pten





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last database update
01/20/2026
MGI 6.24
The Jackson Laboratory