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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Scgb1a1+
wild type
MGI:2437003
Summary 11 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
ht1
Scgb1a1tm1Abm/Scgb1a1+ involves: 129S1/Sv * 129X1/SvJ MGI:6313624
ht2
Scgb1a1tm1(cre/ERT)Blh/Scgb1a1+ involves: 129S4/SvJaeSor * 129S6/SvEv * C57BL/6 MGI:3850367
cn3
Krastm4Tyj/Kras+
Scgb1a1tm1.1(cre)Fjd/Scgb1a1+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:4839215
cn4
Ptentm1Hwu/Ptentm1Hwu
Scgb1a1tm1.1(cre)Fjd/Scgb1a1+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:4839214
cn5
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Scgb1a1tm1.1(cre)Fjd/Scgb1a1+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:4839216
cn6
Krastm4Tyj/Kras+
Scgb1a1tm1(cre)Fjd/Scgb1a1+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 MGI:8226383
cn7
Krastm4Tyj/Kras+
Scgb1a1tm1.1(cre)Fjd/Scgb1a1+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 MGI:8226385
cn8
Foxp1tm1.1Pwt/Foxp1tm1.1Pwt
Foxp4tm2.1Eem/Foxp4tm2.1Eem
Scgb1a1tm1(icre)Fjd/Scgb1a1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:5433107
cn9
Krastm4Tyj/Kras+
Scgb1a1tm1(cre/ERT)Blh/Scgb1a1+
Trp53tm5Tyj/Trp53+
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 MGI:5317170
cn10
Gt(ROSA)26Sortm1(CAG-Sox2,-EGFP)Blh/Gt(ROSA)26Sor+
Scgb1a1tm1(cre/ERT)Blh/Scgb1a1+
involves: 129S6/SvEv * C57BL/6 MGI:4820811
cn11
Gt(ROSA)26Sortm1(CAG-Sox2,-EGFP)Blh/Gt(ROSA)26Sortm1(CAG-Sox2,-EGFP)Blh
Scgb1a1tm1(cre/ERT)Blh/Scgb1a1+
involves: 129S6/SvEv * C57BL/6 MGI:4820809


Genotype
MGI:6313624
ht1
Allelic
Composition
Scgb1a1tm1Abm/Scgb1a1+
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Scgb1a1tm1Abm mutation (0 available); any Scgb1a1 mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• mice exhibit moderate glomerular deposition of IgA

homeostasis/metabolism
• mice exhibit abnormal renal glomerular deposition of complement C3

immune system
• mice exhibit moderate glomerular deposition of IgA
• mice exhibit abnormal renal glomerular deposition of complement C3

renal/urinary system
• mice exhibit moderate glomerular deposition of IgA and deposition of complement C3
• glomeruli exhibit an abnormal deposition of an eosinophilic material which includes fibronectin and collagen




Genotype
MGI:3850367
ht2
Allelic
Composition
Scgb1a1tm1(cre/ERT)Blh/Scgb1a1+
Genetic
Background
involves: 129S4/SvJaeSor * 129S6/SvEv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Scgb1a1tm1(cre/ERT)Blh mutation (1 available); any Scgb1a1 mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• mice are viable and fertile




Genotype
MGI:4839215
cn3
Allelic
Composition
Krastm4Tyj/Kras+
Scgb1a1tm1.1(cre)Fjd/Scgb1a1+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (11 available); any Kras mutation (69 available)
Scgb1a1tm1.1(cre)Fjd mutation (0 available); any Scgb1a1 mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• average survival is 24 weeks

respiratory system
• mutants develop lung lesions that are first detected at 12 weeks of age in alveoli and bronchioles
• mutants develop epithelial lesions termed atypical papillary bronchiolar proliferation that has papillary proliferations of the bronchiolar epithelium located at the bronchiolar terminal site
• however, no carcinomas are seen by 24 weeks of age
• mutants develop lung lesions that are first detected at 12 weeks of age in alveoli and bronchioles
• mutants develop epithelial lesions termed atypical papillary bronchiolar proliferation that has papillary proliferations of the bronchiolar epithelium located at the bronchiolar terminal site
• atypical adenomatous hyperplasia lesions and adenomas

neoplasm
• mutants develop lung lesions that are first detected at 12 weeks of age in alveoli and bronchioles
• mutants develop epithelial lesions termed atypical papillary bronchiolar proliferation that has papillary proliferations of the bronchiolar epithelium located at the bronchiolar terminal site
• atypical adenomatous hyperplasia lesions and adenomas




Genotype
MGI:4839214
cn4
Allelic
Composition
Ptentm1Hwu/Ptentm1Hwu
Scgb1a1tm1.1(cre)Fjd/Scgb1a1+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Hwu mutation (17 available); any Pten mutation (86 available)
Scgb1a1tm1.1(cre)Fjd mutation (0 available); any Scgb1a1 mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• mice are viable and exhibit not visible abnormalities and remain healthy throughout 12 months of study, with normal lungs




Genotype
MGI:4839216
cn5
Allelic
Composition
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Scgb1a1tm1.1(cre)Fjd/Scgb1a1+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (11 available); any Kras mutation (69 available)
Ptentm1Hwu mutation (17 available); any Pten mutation (86 available)
Scgb1a1tm1.1(cre)Fjd mutation (0 available); any Scgb1a1 mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mean survival is 8 weeks

immune system
• increase in inflammation in lesions compared to single Kras mutants, with an increase in neutrophil and endothelial cell infiltration; infiltration of these cells increases with malignant progression

respiratory system
• increase in inflammation in lesions compared to single Kras mutants, with an increase in neutrophil and endothelial cell infiltration; infiltration of these cells increases with malignant progression
• mutants have higher numbers of lesions and more extensive tumors than single Kras mutants
• mutants develop distinct bronchial and alveolar tumors
• mutants develop lung lesions as early as 4 weeks of age including proliferative atypical adenomatous hyperplasia lesions
• mutants develop lung lesions as early as 4 weeks of age that includes atypical papillary bronchiolar proliferation
• mucinous bronchioloalveolar cell carcinoma-like lesions, a subtype of lung adenocarcinoma
• by 2 months of age, mutants exhibit tachypnea

neoplasm
• mutants have higher numbers of lesions and more extensive tumors than single Kras mutants
• mutants develop distinct bronchial and alveolar tumors
• mutants develop lung lesions as early as 4 weeks of age including proliferative atypical adenomatous hyperplasia lesions
• mutants develop lung lesions as early as 4 weeks of age that includes atypical papillary bronchiolar proliferation
• mucinous bronchioloalveolar cell carcinoma-like lesions, a subtype of lung adenocarcinoma

growth/size/body
• by 2 months of age, mutants exhibit weight loss




Genotype
MGI:8226383
cn6
Allelic
Composition
Krastm4Tyj/Kras+
Scgb1a1tm1(cre)Fjd/Scgb1a1+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (11 available); any Kras mutation (69 available)
Scgb1a1tm1(cre)Fjd mutation (0 available); any Scgb1a1 mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• shortened life span, with a median survival time of 10 months and no mice surviving past 12 months of age
• shortened life span due to lung tumors

neoplasm
• the main lesions are epithelial hyperplasia in the early stage and adenomas in the middle and late stages
• isolated small lesions in the lungs are seen in 4- and 6-month-old mice and an increase in lesion size is seen with age
• however, no lesions are seen in other organs, including brain, liver, kidney, intestine, and muscle and no metastases are seen
• lesions are atypical papillary bronchiolar hyperplasia, solid and papillary adenomas, adenomas with atypical cytologic features, atypical papillary bronchiolar hyperplasia adjacent to adenomas, and adenoncarcinoma
• lesions include solid and papillary adenomas and adenomas with atypical cytologic features
• adenomas are predominately of the papillary subtype
• number of adenomas is less than in Krastm4Tyj Scgb1a1tm1.1(cre)Fjd mice but the mean size of adenomas is greater
• adenocarcinomas are only seen in the very late stage

respiratory system
• focal to extensive acidophilic pneumonia is seen surrounding adenomas and adenocarcinomas in 30% of the total lung tumors
• isolated small lesions in the lungs are seen in 4- and 6-month-old mice and an increase in lesion size is seen with age
• however, no lesions are seen in other organs, including brain, liver, kidney, intestine, and muscle and no metastases are seen
• lesions are atypical papillary bronchiolar hyperplasia, solid and papillary adenomas, adenomas with atypical cytologic features, atypical papillary bronchiolar hyperplasia adjacent to adenomas, and adenoncarcinoma
• the main lesions are epithelial hyperplasia in the early stage and adenomas in the middle and late stages
• lesions include solid and papillary adenomas and adenomas with atypical cytologic features
• adenomas are predominately of the papillary subtype
• number of adenomas is less than in Krastm4Tyj Scgb1a1tm1.1(cre)Fjd mice but the mean size of adenomas is greater
• adenocarcinomas are only seen in the very late stage
• lesions include atypical papillary bronchiolar hyperplasia and atypical papillary bronchiolar hyperplasia adjacent to adenomas
• in early stages, epithelial hyperplasia is only seen in bronchioles, not in the alveolar sac area

immune system
• focal to extensive acidophilic pneumonia is seen surrounding adenomas and adenocarcinomas in 30% of the total lung tumors

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
lung cancer DOID:1324 OMIM:211980
OMIM:608935
OMIM:612571
OMIM:612593
OMIM:614210
J:159271




Genotype
MGI:8226385
cn7
Allelic
Composition
Krastm4Tyj/Kras+
Scgb1a1tm1.1(cre)Fjd/Scgb1a1+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (11 available); any Kras mutation (69 available)
Scgb1a1tm1.1(cre)Fjd mutation (0 available); any Scgb1a1 mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• shortened life span, with a median survival time of 6 months and no mice surviving past 8 months of age
• shortened life span due to lung tumors

neoplasm
• weekly exposure to aerosolized nontypeable Haemophilus influenzae lystate (NTHi) for 8 weeks to induce chronic obstructive pulmonary disease (COPD)-like chronic airway inflammation increases lung surface tumors 3.2-fold while no tumors are seen in NTHi treated wild-type mice
• isolated small lesions in the lungs are seen in 1- and 2-month-old mice and an increase in lesion size is seen with age
• however, no lesions are seen in other organs, including brain, liver, kidney, intestine, and muscle and no metastases are seen
• lesions are atypical papillary bronchiolar hyperplasia, solid and papillary adenomas, adenomas with atypical cytologic features, atypical papillary bronchiolar hyperplasia adjacent to adenomas, and adenoncarcinoma
• the main lesions are epithelial hyperplasia in the early stage and adenomas in the middle and late stages
• early lung lesions exhibit a Clara cell phenotype indicating that lesions come from Clara Cells of conducting airways and more advanced pathologies show an alveolar type II cell phenotype
• weekly exposure to aerosolized nontypable Haemophilus influenzae lysate results in an increase in total lung tumor burden
• lesions include solid and papillary adenomas and adenomas with atypical cytologic features
• adenomas are predominately of the papillary subtype
• number of adenomas is greater than in Krastm4Tyj Scgb1a1tm1(cre)Fjd mice but the mean size of adenomas is smaller

respiratory system
• mice show elevated macrophage numbers in bronchoalveolar lavage fluid (BALF)
• 14-week-old mice show focal infiltration of macrophages around hyperplastic and adenomatous lesions
• focal to extensive acidophilic pneumonia is seen surrounding adenomas and adenocarcinomas in 30% of the total lung tumors
• mice exposed to aerosolized nontypeable Haemophilus influenzae lystate (NTHi) once weekly for 8 weeks to induce chronic obstructive pulmonary disease (COPD)-like chronic airway inflammation show dense infiltration of the lung parenchyma with macrophages, neutrophils, and lymphocytes indicating neutrophil/macrophage/CD8 T cell-associated COPD-like airway inflammation; the inflammatory infiltrate is centered around airways and blood vessels, but also extends widely into alveolar spaces
• isolated small lesions in the lungs are seen in 1- and 2-month-old mice and an increase in lesion size is seen with age
• however, no lesions are seen in other organs, including brain, liver, kidney, intestine, and muscle and no metastases are seen
• lesions are atypical papillary bronchiolar hyperplasia, solid and papillary adenomas, adenomas with atypical cytologic features, atypical papillary bronchiolar hyperplasia adjacent to adenomas, and adenoncarcinoma
• the main lesions are epithelial hyperplasia in the early stage and adenomas in the middle and late stages
• early lung lesions exhibit a Clara cell phenotype indicating that lesions come from Clara Cells of conducting airways and more advanced pathologies show an alveolar type II cell phenotype
• weekly exposure to aerosolized nontypable Haemophilus influenzae lysate results in an increase in total lung tumor burden
• lesions include solid and papillary adenomas and adenomas with atypical cytologic features
• adenomas are predominately of the papillary subtype
• number of adenomas is greater than in Krastm4Tyj Scgb1a1tm1(cre)Fjd mice but the mean size of adenomas is smaller
• in early stages, epithelial hyperplasia is only seen in bronchioles, not in the alveolar sac area
• lesions include atypical papillary bronchiolar hyperplasia and atypical papillary bronchiolar hyperplasia adjacent to adenomas

immune system
• mice show elevated macrophage numbers in bronchoalveolar lavage fluid (BALF)
• 14-week-old mice show focal infiltration of macrophages around hyperplastic and adenomatous lesions
• focal to extensive acidophilic pneumonia is seen surrounding adenomas and adenocarcinomas in 30% of the total lung tumors
• mice exposed to aerosolized nontypeable Haemophilus influenzae lystate (NTHi) once weekly for 8 weeks to induce chronic obstructive pulmonary disease (COPD)-like chronic airway inflammation show dense infiltration of the lung parenchyma with macrophages, neutrophils, and lymphocytes indicating neutrophil/macrophage/CD8 T cell-associated COPD-like airway inflammation; the inflammatory infiltrate is centered around airways and blood vessels, but also extends widely into alveolar spaces

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
lung cancer DOID:1324 OMIM:211980
OMIM:608935
OMIM:612571
OMIM:612593
OMIM:614210
J:159271




Genotype
MGI:5433107
cn8
Allelic
Composition
Foxp1tm1.1Pwt/Foxp1tm1.1Pwt
Foxp4tm2.1Eem/Foxp4tm2.1Eem
Scgb1a1tm1(icre)Fjd/Scgb1a1+
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxp1tm1.1Pwt mutation (1 available); any Foxp1 mutation (77 available)
Foxp4tm2.1Eem mutation (0 available); any Foxp4 mutation (89 available)
Scgb1a1tm1(icre)Fjd mutation (1 available); any Scgb1a1 mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• mice exhibit an increase in goblet cell differentiation compared with control mice
• following naphthalene injury, mice exhibit defective epithelial regeneration by ectopically activating goblet cell fate compared with control mice

homeostasis/metabolism
• following naphthalene injury, mice exhibit defective epithelial regeneration by ectopically activating goblet cell fate compared with control mice




Genotype
MGI:5317170
cn9
Allelic
Composition
Krastm4Tyj/Kras+
Scgb1a1tm1(cre/ERT)Blh/Scgb1a1+
Trp53tm5Tyj/Trp53+
Genetic
Background
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (11 available); any Kras mutation (69 available)
Scgb1a1tm1(cre/ERT)Blh mutation (1 available); any Scgb1a1 mutation (31 available)
Trp53tm5Tyj mutation (1 available); any Trp53 mutation (237 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• animal succumb due to tumor burden at 20-24 weeks

neoplasm
• at 6-8 weeks of age, animals administered 4 doses of tamoxifen develop adenomas in the alveoli by 15 weeks; these progress to adenocarcinomas
• papillary adenomas are seen in alveoli at 15 and 21 weeks after tamoxifen treatment
• develop in alveoli and near the bronchioalveolar duct junction by 15 weeks of age with tamoxifen administration at 6-8 weeks
• larger bronchioles and non terminal bronchi appear normal
• advanced papillary adenocarcinomas are observed at 21 weeks after tamoxifen treatment

respiratory system
• at 6-8 weeks of age, animals administered 4 doses of tamoxifen develop adenomas in the alveoli by 15 weeks; these progress to adenocarcinomas
• papillary adenomas are seen in alveoli at 15 and 21 weeks after tamoxifen treatment
• hyperplasia is observed at 3 weeks after tamoxifen induction, and persists at 15 and 21 weeks




Genotype
MGI:4820811
cn10
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-Sox2,-EGFP)Blh/Gt(ROSA)26Sor+
Scgb1a1tm1(cre/ERT)Blh/Scgb1a1+
Genetic
Background
involves: 129S6/SvEv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-Sox2,-EGFP)Blh mutation (0 available); any Gt(ROSA)26Sor mutation (1083 available)
Scgb1a1tm1(cre/ERT)Blh mutation (1 available); any Scgb1a1 mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• after 13 weeks of tamoxifen treatment, mice exhibit bronchial epithelial hyperplasia unlike wild-type control mice
• however, areas of hyperplasia do not progress to cancer after 18 weeks of tamoxifen treatment

neoplasm
N
• areas of hyperplasia do not progress to cancer after 18 weeks of tamoxifen treatment




Genotype
MGI:4820809
cn11
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-Sox2,-EGFP)Blh/Gt(ROSA)26Sortm1(CAG-Sox2,-EGFP)Blh
Scgb1a1tm1(cre/ERT)Blh/Scgb1a1+
Genetic
Background
involves: 129S6/SvEv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-Sox2,-EGFP)Blh mutation (0 available); any Gt(ROSA)26Sor mutation (1083 available)
Scgb1a1tm1(cre/ERT)Blh mutation (1 available); any Scgb1a1 mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• at 12 to 34 weeks of tamoxifen treatment, 50% of mice exhibit well-defined adenocarcinomas unlike wild-type control mice
• after 6 weeks of tamoxifen treatment, mice exhibit bronchial epithelial hyperplasia unlike wild-type control mice

neoplasm
• at 12 to 34 weeks of tamoxifen treatment, 50% of mice exhibit well-defined adenocarcinomas unlike wild-type control mice





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