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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID 		Braftm1Mmcm
targeted mutation 1, Martin McMahon
MGI:3711771
Summary 24 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
ht1
 		Braftm1Mmcm/Braf+ involves: 129P2/OlaHsd MGI:3712025
cn2
 		Braftm1Mmcm/Braf+ involves: 129P2/OlaHsd MGI:3712021
cn3
 		Braftm1Mmcm/Braf+ involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5897856
cn4
 		Braftm1Mmcm/Braf+
Ptentm1Mro/Ptentm1Mro
Tg(Tyr-cre/ERT2)1Lru/0 		B6.Cg-Braftm1Mmcm Tg(Tyr-cre/ERT2)1Lru Ptentm1Mro MGI:5447169
cn5
 		Braftm1Mmcm/Braf+
Ezh2tm1.1Nesh/Ezh2+
Tg(Tyr-cre/ERT2)13Bos/0 		involves: 129 * 129P2/OlaHsd * C57BL/6 * FVB MGI:6393921
cn6
 		Braftm1Mmcm/Braf+
Tg(Tg-cre/ERT2)#Mmcm/0 		involves: 129P2/OlaHsd MGI:5780077
cn7
 		Braftm1Mmcm/Braf+
Cdkn2atm4Rdp/Cdkn2atm4Rdp 		involves: 129P2/OlaHsd MGI:3712026
cn8
 		Braftm1Mmcm/Braf+
Trp53tm1Brn/Trp53tm1Brn 		involves: 129P2/OlaHsd MGI:3712022
cn9
 		Braftm1Mmcm/Braf+
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Tyr-cre/ERT2)13Bos/0 		involves: 129P2/OlaHsd * 129S1/Sv * FVB MGI:5902129
cn10
 		Braftm1Mmcm/Braf+
Ptentm2.1Ppp/Pten+
Tg(Tyr-cre/ERT2)13Bos/0 		involves: 129P2/OlaHsd * 129S1/Sv * FVB MGI:5902136
cn11
 		Braftm1Mmcm/Braftm1Mmcm
Nkx3-1tm4(cre/ERT2)Mms/Nkx3-1+
Ptentm1Hwu/Pten+ 		involves: 129P2/OlaHsd * 129S4/SvJae * 129S6/SvEvTac * C57BL/6 MGI:5543907
cn12
 		Braftm1Mmcm/Braftm1Mmcm
Cd207tm2.1(cre)Bjec/Cd207+ 		involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:6192274
cn13
 		Braftm1Mmcm/Braf+
Trp53tm1Brn/Trp53tm3.1Tyj
Tg(TPO-cre/ERT2)1139Tyj/0 		involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * C57BL/6NTac MGI:5897858
cn14
 		Braftm1Mmcm/Braf+
Tg(TPO-cre/ERT2)1139Tyj/0 		involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * C57BL/6NTac MGI:5897855
cn15
 		Braftm1Mmcm/Braf+
Trp53tm3.1Tyj/Trp53+
Tg(TPO-cre/ERT2)1139Tyj/0 		involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * C57BL/6NTac MGI:5897857
cn16
 		Braftm1Mmcm/Braf+
Tg(TPO-cre/ERT2)1139Tyj/0
Trp53tm1Brn/Trp53tm1Brn 		involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * C57BL/6NTac MGI:5897859
cn17
 		Braftm1Mmcm/Braf+
Ptentm1Rdp/Ptentm1Rdp
Tg(Tyr-cre/ERT2)13Bos/0 		involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * FVB/N MGI:5902132
cn18
 		Braftm1Mmcm/Braftm1Mmcm
Tg(Itgax-cre)1-1Reiz/0 		involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:6192275
cn19
 		Braftm1Mmcm/Braf+
Tg(Tyr-cre/ERT2)13Bos/0 		involves: 129P2/OlaHsd * C57BL/6 * FVB MGI:6393928
cn20
 		Braftm1Mmcm/Braf+
Polr2atm1(cre/ERT2)Bbd/Polr2a+ 		involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:3712024
cn21
 		Braftm1Mmcm/Braftm1Mmcm
Tg(Tyr-cre/ERT2)13Bos/0 		involves: 129P2/OlaHsd * FVB MGI:5902126
cn22
 		Braftm1Mmcm/Braf+
Tg(Tyr-cre/ERT2)13Bos/0 		involves: 129P2/OlaHsd * FVB MGI:5902125
cn23
 		Braftm1Mmcm/?
Tg(TPO-cre)1Shk/0 		involves: 129P2/OlaHsd * FVB/NCr MGI:5780076
cn24
 		Braftm1Mmcm/Braf+
Gt(ROSA)26Sortm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Tg(Mitf-cre)7114Gsb/0 		STOCK Braftm1Mmcm Gt(ROSA)26Sortm14(CAG-tdTomato)Hze Tg(Mitf-cre)7114Gsb/Cvrk MGI:6792072


Genotype
MGI:3712025
ht1
Allelic
Composition		 Braftm1Mmcm/Braf+
Genetic
Background		 involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
normal phenotype
no abnormal phenotype detected ( J:121715 )
• mice are fertile and born at Mendelian ratios, but no further phenotypic analysis is provided




Genotype
MGI:3712021
cn2
Allelic
Composition		 Braftm1Mmcm/Braf+
Genetic
Background		 involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
mortality/aging
premature death ( J:121715 )
• 7-8 weeks after adenoviral Cre intranasal administration to 6- to 8-week old mutants, treated animals are euthanized because they show labored breathing and general wasting

neoplasm
increased lung tumor incidence ( J:121715 )
• cellular origins of cancerous are ambiguous aslesions are Clara Cell antigen-negative, but majority of cells express Surfactant protein C as early as 2 weeks after Cre treatment (CCA and SP-C are both markers of alveolar type II pneumocytes)
• 4 weeks after Cre treatment, mice are treated for 28 days with a pharmacological inhibitor of MEK1/2 which prevents almost all tumor development, while vehicle-treated animals show numerous lung tumors
increased lung adenoma incidence ( J:121715 )
• 7 weeks after high dose Cre treatment, evidence of multiple adenomatous tumor formation is present in mouse lungs, while no tumors are detected in untreated mice after 6 months
• papillary adenomas are detected 6-8 weeks after lower dose adenoviral Cre treatment; lesions seem to increase in size and number
• lesions arise in alveolar ducts expanding outward and around broncioles
• at ~14 weeks, papillary adenomas undergo changes at periphery; cells change such that they have more cytoplasm and become eosinophilic
• after lower dose Cre treatement, adenomas do not grow beyond ~900 um in diameter
increased lung adenocarcinoma incidence ( J:121715 )
• only 2 mice (of 57) that develop adenomas show evidence of progression to adenocarcinoma; cells from these mice display nuclear enlargement, hyperchromasia, and contour irregularities

respiratory system
increased lung tumor incidence ( J:121715 )
• cellular origins of cancerous are ambiguous aslesions are Clara Cell antigen-negative, but majority of cells express Surfactant protein C as early as 2 weeks after Cre treatment (CCA and SP-C are both markers of alveolar type II pneumocytes)
• 4 weeks after Cre treatment, mice are treated for 28 days with a pharmacological inhibitor of MEK1/2 which prevents almost all tumor development, while vehicle-treated animals show numerous lung tumors
increased lung adenoma incidence ( J:121715 )
• 7 weeks after high dose Cre treatment, evidence of multiple adenomatous tumor formation is present in mouse lungs, while no tumors are detected in untreated mice after 6 months
• papillary adenomas are detected 6-8 weeks after lower dose adenoviral Cre treatment; lesions seem to increase in size and number
• lesions arise in alveolar ducts expanding outward and around broncioles
• at ~14 weeks, papillary adenomas undergo changes at periphery; cells change such that they have more cytoplasm and become eosinophilic
• after lower dose Cre treatement, adenomas do not grow beyond ~900 um in diameter
increased lung adenocarcinoma incidence ( J:121715 )
• only 2 mice (of 57) that develop adenomas show evidence of progression to adenocarcinoma; cells from these mice display nuclear enlargement, hyperchromasia, and contour irregularities
lung epithelium hyperplasia ( J:121715 )
• 4 weeks after Cre administration, lung epithelium hyperplasia is observed
• at earlier times after Cre treatment, hyperplastic epithelium shows papillary outgrowths, but these were not seen at earlier time points (2-4 weeks post-treatment)




Genotype
MGI:5897856
cn3
Allelic
Composition		 Braftm1Mmcm/Braf+
Genetic
Background		 involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
endocrine/exocrine glands
increased thyroid carcinoma incidence ( J:208854 )
• mice with surgical delivery of a cre-expressing adenovirus to the adult thyroid gland develop papillary thyroid carcinoma

neoplasm
increased thyroid carcinoma incidence ( J:208854 )
• mice with surgical delivery of a cre-expressing adenovirus to the adult thyroid gland develop papillary thyroid carcinoma




Genotype
MGI:5447169
cn4
Allelic
Composition		 Braftm1Mmcm/Braf+
Ptentm1Mro/Ptentm1Mro
Tg(Tyr-cre/ERT2)1Lru/0
Genetic
Background		 B6.Cg-Braftm1Mmcm Tg(Tyr-cre/ERT2)1Lru Ptentm1Mro
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
Ptentm1Mro mutation (1 available); any Pten mutation (88 available)
Tg(Tyr-cre/ERT2)1Lru mutation (1 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
mortality/aging
premature death ( J:188523 )
• tamoxifen-treated mice must be euthanized between 40 and 70 days due to tumor load or ulceration
decreased tumor-free survival time ( J:188523 )
• in tamoxifen treated mice

neoplasm
increased cutaneous melanoma incidence ( J:188523 )
• tamoxifen-treated mice develop multiple heavily pigmented papules with an average latency of 18 days
• tamoxifen-treated mice exhibit metastasis in draining lymph nodes as early as 4 weeks after tumor induction
• however, no visceral metastasis is observed
• however, treatment with PLX4720 decreases tumor outgrowth
• in the absences of tamoxifen, most mice develop spontaneous melanomas due to leaky cre expression

integument
spontaneous skin ulceration ( J:188523 )
• in tamoxifen-treated mice
increased cutaneous melanoma incidence ( J:188523 )
• tamoxifen-treated mice develop multiple heavily pigmented papules with an average latency of 18 days
• tamoxifen-treated mice exhibit metastasis in draining lymph nodes as early as 4 weeks after tumor induction
• however, no visceral metastasis is observed
• however, treatment with PLX4720 decreases tumor outgrowth
• in the absences of tamoxifen, most mice develop spontaneous melanomas due to leaky cre expression




Genotype
MGI:6393921
cn5
Allelic
Composition		 Braftm1Mmcm/Braf+
Ezh2tm1.1Nesh/Ezh2+
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background		 involves: 129 * 129P2/OlaHsd * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
Ezh2tm1.1Nesh mutation (1 available); any Ezh2 mutation (72 available)
Tg(Tyr-cre/ERT2)13Bos mutation (12 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
neoplasm
increased melanoma incidence ( J:239472 )
• tamoxifen-treated mice show accelerated tumorigenesis of unpigmented, nonmetastatic melanoma compared to single Braf conditional mutants




Genotype
MGI:5780077
cn6
Allelic
Composition		 Braftm1Mmcm/Braf+
Tg(Tg-cre/ERT2)#Mmcm/0
Genetic
Background		 involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
Tg(Tg-cre/ERT2)#Mmcm mutation (0 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
neoplasm
increased thyroid carcinoma incidence ( J:172205 )
• mice develop extensive papillary thyroid carcinomas by 12 months of tamoxifen treatment, first showing enlarged follicles within 7 days of tamoxifen treatment, a squamous morphology of thyrocytes accompanied by a large increase in follicle size and loss of colloid by 14 days of tamoixfen treatment, and tumor cells with characteristic papillary structure by 6 months of tamoxifen administration
• occasionally localized tumor invasion into the surrounding muscle is seen, however frank metastasis to lymph nodes or distant organs is not observed
• although mice have palpable thyroid tumors by 13 months of tamoxifen treatment, mice are not overtly sick
• mice not treated with tamoxifen show regions of papillary thyroid cancer with adjacent histologically normal thyroid architecture at 12 months of age, however these mice exhibit normal TSH and T4 levels
• treatment with PD0325901, an MEK1/2 inhibitor, results in regression of papillary thyroid cancer in tamoxifen-administered mutants
• treatment with PD0325901 and T3 results in further papillary thyroid cancer regression in tamoxifen-administered mutants

endocrine/exocrine glands
abnormal thyroid gland morphology ( J:172205 )
• mice not treated with tamoxifen exhibit increased thyroid volume, however thyroid architecture is normal, indicating some leakiness of the cre transgene
abnormal thyroid follicle morphology ( J:172205 )
• within 7 days of tamoxifen treatment, mice show enlarged follicles throughout the entire gland
enlarged thyroid gland ( J:172205 )
• treatment with PD0325901 leads to decreased thyroid size of tamoxifen-administered mice
• tamoxifen treated mice develop an enlarged, goiterous, hypercellular thyroid that is up to 10 times larger than controls at 1 month and up to 300 times larger at 12 months after tamoxifen treatment
increased thyroid carcinoma incidence ( J:172205 )
• mice develop extensive papillary thyroid carcinomas by 12 months of tamoxifen treatment, first showing enlarged follicles within 7 days of tamoxifen treatment, a squamous morphology of thyrocytes accompanied by a large increase in follicle size and loss of colloid by 14 days of tamoixfen treatment, and tumor cells with characteristic papillary structure by 6 months of tamoxifen administration
• occasionally localized tumor invasion into the surrounding muscle is seen, however frank metastasis to lymph nodes or distant organs is not observed
• although mice have palpable thyroid tumors by 13 months of tamoxifen treatment, mice are not overtly sick
• mice not treated with tamoxifen show regions of papillary thyroid cancer with adjacent histologically normal thyroid architecture at 12 months of age, however these mice exhibit normal TSH and T4 levels
• treatment with PD0325901, an MEK1/2 inhibitor, results in regression of papillary thyroid cancer in tamoxifen-administered mutants
• treatment with PD0325901 and T3 results in further papillary thyroid cancer regression in tamoxifen-administered mutants
decreased activity of thyroid gland ( J:172205 )
• mice develop hypothyroidism by 1-3 months of tamoxifen treatment

homeostasis/metabolism
decreased circulating thyroxine level ( J:172205 )
• mice exhibit a decrease in serum T4 levels at 1 and 3 months of tamoxifen treatment
• mice not treated with tamoxifen exhibit normal T4 levels
increased circulating thyroid-stimulating hormone level ( J:172205 )
• 100-fold increase in serum TSH levels at 1 and 3 months of tamoxifen treatment
• mice not treated with tamoxifen exhibit normal levels of TSH

Mouse Models of Human Disease
 DO ID OMIM ID(s) Ref(s)
papillary thyroid carcinoma DOID:3969 OMIM:188550
 J:172205




Genotype
MGI:3712026
cn7
Allelic
Composition		 Braftm1Mmcm/Braf+
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Genetic
Background		 involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
Cdkn2atm4Rdp mutation (0 available); any Cdkn2a mutation (67 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
neoplasm
increased lung tumor incidence ( J:121715 )
• Cre-treated mice show scattered papillary adenomas with evidence of subpleural nodules harboring cords of atypical cells trapped within regions of mesenchymal proliferation
• 2/4 mice display multiple lung tumors with a bronchioalveolar component

respiratory system
increased lung tumor incidence ( J:121715 )
• Cre-treated mice show scattered papillary adenomas with evidence of subpleural nodules harboring cords of atypical cells trapped within regions of mesenchymal proliferation
• 2/4 mice display multiple lung tumors with a bronchioalveolar component




Genotype
MGI:3712022
cn8
Allelic
Composition		 Braftm1Mmcm/Braf+
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background		 involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
neoplasm
increased lung tumor incidence ( J:121715 )
• 8 weeks after adenoCre treatment, lungs show rapid cancer progression with increased proliferation compared to Trp53-sufficient mice
• tumors show nodules composed of central papillary structures with solid peripheral areas
• all double mutants show increased proliferation, and cells show altered nuclear morphology, while Trp53 conditional single mutants have normal lung phenotypes
increased lung adenocarcinoma incidence ( J:121715 )
• 2/5 mice are found to have prominent adenocarcinomas, composed of glandular structures lined by atypical cells with enlarged nuclei, hyperchromasia, contour irregularities, and prominent nucleoli
• large areas of necrosis are present in adenocarcinomas, with evidence of lymphatic and vascular invasion

respiratory system
abnormal lung morphology ( J:121715 )
• 8 weeks after Cre treatment, some small airways display papillary hyperplasia, not seen in Braf-conditional mice
increased lung tumor incidence ( J:121715 )
• 8 weeks after adenoCre treatment, lungs show rapid cancer progression with increased proliferation compared to Trp53-sufficient mice
• tumors show nodules composed of central papillary structures with solid peripheral areas
• all double mutants show increased proliferation, and cells show altered nuclear morphology, while Trp53 conditional single mutants have normal lung phenotypes
increased lung adenocarcinoma incidence ( J:121715 )
• 2/5 mice are found to have prominent adenocarcinomas, composed of glandular structures lined by atypical cells with enlarged nuclei, hyperchromasia, contour irregularities, and prominent nucleoli
• large areas of necrosis are present in adenocarcinomas, with evidence of lymphatic and vascular invasion




Genotype
MGI:5902129
cn9
Allelic
Composition		 Braftm1Mmcm/Braf+
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background		 involves: 129P2/OlaHsd * 129S1/Sv * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
Ptentm2.1Ppp mutation (0 available); any Pten mutation (88 available)
Tg(Tyr-cre/ERT2)13Bos mutation (12 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
integument
increased cutaneous melanoma incidence ( J:151023 )
• 7-10 days following 4-hydroxytamoxifen (4-HT) treatment, all mice show expansion of highly pigmented cells that develop into pigmented malignant lesions in locations of 4-HT administration such as the face, flank, or tail skin
• pigmented melanoma cells are seen throughout the dermis and subcutis of 4-HT treated mice and show pagetoid spread into the epidermis
• lesions in 4-HT treated mice progress rapidly to advanced malignancy such that all mice require euthanasia 25-50 days following 4-HT administration
• treatment of 4-HT treated mice with the MEK1/2 inhibitor PD325901 or the mTorc1 inhibitor rapamycin inhibits melanoma formation
• mice in which drug treatment is ceased subsequently develop malignant melanoma
• mice treated once with PD325901 to prevent melanoma remain sensitive to the anti-melanoma action of a second round of PD325901 administration

neoplasm
increased cutaneous melanoma incidence ( J:151023 )
• 7-10 days following 4-hydroxytamoxifen (4-HT) treatment, all mice show expansion of highly pigmented cells that develop into pigmented malignant lesions in locations of 4-HT administration such as the face, flank, or tail skin
• pigmented melanoma cells are seen throughout the dermis and subcutis of 4-HT treated mice and show pagetoid spread into the epidermis
• lesions in 4-HT treated mice progress rapidly to advanced malignancy such that all mice require euthanasia 25-50 days following 4-HT administration
• treatment of 4-HT treated mice with the MEK1/2 inhibitor PD325901 or the mTorc1 inhibitor rapamycin inhibits melanoma formation
• mice in which drug treatment is ceased subsequently develop malignant melanoma
• mice treated once with PD325901 to prevent melanoma remain sensitive to the anti-melanoma action of a second round of PD325901 administration
increased metastatic potential ( J:151023 )
• spread of melanoma in 4-HT treated mice is seen into the regional draining lymph nodes in 100% of mice and to the lungs in some cases

Mouse Models of Human Disease
 DO ID OMIM ID(s) Ref(s)
skin melanoma DOID:8923 OMIM:608035
OMIM:612263
 J:151023




Genotype
MGI:5902136
cn10
Allelic
Composition		 Braftm1Mmcm/Braf+
Ptentm2.1Ppp/Pten+
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background		 involves: 129P2/OlaHsd * 129S1/Sv * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
Ptentm2.1Ppp mutation (0 available); any Pten mutation (88 available)
Tg(Tyr-cre/ERT2)13Bos mutation (12 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
integument
increased cutaneous melanoma incidence ( J:151023 )
• 4-HT treated mice eventually develop focal malignant melanomas

neoplasm
increased cutaneous melanoma incidence ( J:151023 )
• 4-HT treated mice eventually develop focal malignant melanomas

pigmentation
abnormal melanocyte morphology ( J:151023 )
• 4-hydroxytamoxifen (4-HT) treated mice initially develop benign melanocytic lesions but they eventually develop focal malignant melanomas




Genotype
MGI:5543907
cn11
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 (3 available); any Braf mutation (60 available)
Nkx3-1tm4(cre/ERT2)Mms mutation (14 available); any Nkx3-1 mutation (38 available)
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
mortality/aging
premature death ( J:191327 )
• mutants develop lethal prostate cancer 4 months after tamoxifen induction

neoplasm
increased prostate gland tumor incidence ( J:191327 )
• 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
increased prostate gland adenocarcinoma incidence ( J:191327 )
• tamoxifen treated mutants develop invasive adenocarcinoma by 2-3 months after tamoxifen induction
increased prostate intraepithelial neoplasia incidence ( J:191327 )
• tamoxifen treated mutants display prostate intraepithelial neoplasia (PIN) by 2-4 weeks after tamoxifen induction
increased metastatic potential ( J:191327 )
• 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
increased prostate gland tumor incidence ( J:191327 )
• 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
increased prostate gland adenocarcinoma incidence ( J:191327 )
• tamoxifen treated mutants develop invasive adenocarcinoma by 2-3 months after tamoxifen induction
increased prostate intraepithelial neoplasia incidence ( J:191327 )
• tamoxifen treated mutants display prostate intraepithelial neoplasia (PIN) by 2-4 weeks after tamoxifen induction

reproductive system
increased prostate gland tumor incidence ( J:191327 )
• 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
increased prostate gland adenocarcinoma incidence ( J:191327 )
• tamoxifen treated mutants develop invasive adenocarcinoma by 2-3 months after tamoxifen induction
increased prostate intraepithelial neoplasia incidence ( J:191327 )
• tamoxifen treated mutants display prostate intraepithelial neoplasia (PIN) by 2-4 weeks after tamoxifen induction




Genotype
MGI:6192274
cn12
Allelic
Composition		 Braftm1Mmcm/Braftm1Mmcm
Cd207tm2.1(cre)Bjec/Cd207+
Genetic
Background		 involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
Cd207tm2.1(cre)Bjec mutation (0 available); any Cd207 mutation (25 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
hematopoietic system
increased dendritic cell number ( J:211690 )
• increase in number of mainly MHC II+CD11c+ dendritic cells in the liver
• however, the number of dendritic cells in the lung and total numbers of macrophages, NK cells, B cells, and T cells are unaffected and mice do not exhibit anemia or alternation of circulating blood dendritic cells numbers

immune system
increased dendritic cell number ( J:211690 )
• increase in number of mainly MHC II+CD11c+ dendritic cells in the liver
• however, the number of dendritic cells in the lung and total numbers of macrophages, NK cells, B cells, and T cells are unaffected and mice do not exhibit anemia or alternation of circulating blood dendritic cells numbers
liver inflammation ( J:211690 )
• by 12 weeks of age, mice develop small inflammatory infiltrates mainly to the liver that progressively increase in size with age
lung inflammation ( J:211690 )
• by 20 weeks of age, all mice show small lesions in the lung

liver/biliary system
liver inflammation ( J:211690 )
• by 12 weeks of age, mice develop small inflammatory infiltrates mainly to the liver that progressively increase in size with age

respiratory system
lung inflammation ( J:211690 )
• by 20 weeks of age, all mice show small lesions in the lung

Mouse Models of Human Disease
 DO ID OMIM ID(s) Ref(s)
Langerhans-cell histiocytosis DOID:2571 OMIM:246400
OMIM:604856
 J:211690




Genotype
MGI:5897858
cn13
Allelic
Composition		 Braftm1Mmcm/Braf+
Trp53tm1Brn/Trp53tm3.1Tyj
Tg(TPO-cre/ERT2)1139Tyj/0
Genetic
Background		 involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
Tg(TPO-cre/ERT2)1139Tyj mutation (1 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
Trp53tm3.1Tyj mutation (2 available); any Trp53 mutation (240 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
endocrine/exocrine glands
increased thyroid carcinoma incidence ( J:208854 )
• tamoxifen treated mice exhibit accelerated progression to poorly differentiated thyroid carcinoma and overt undifferentiated anaplastic thyroid carcinoma with highly pleomorphic, atypical cells with evidence of necrosis

neoplasm
increased thyroid carcinoma incidence ( J:208854 )
• tamoxifen treated mice exhibit accelerated progression to poorly differentiated thyroid carcinoma and overt undifferentiated anaplastic thyroid carcinoma with highly pleomorphic, atypical cells with evidence of necrosis




Genotype
MGI:5897855
cn14
Allelic
Composition		 Braftm1Mmcm/Braf+
Tg(TPO-cre/ERT2)1139Tyj/0
Genetic
Background		 involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
Tg(TPO-cre/ERT2)1139Tyj mutation (1 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
endocrine/exocrine glands
increased thyroid carcinoma incidence ( J:208854 )
• mice administered tamoxifen develop papillary thyroid carcinomas
• tumors show both papillary growth morphology and nuclear features of papillary thyroid carcinoma
• even with very long latency, extrathyroidal invasion is not seen and cervical lymph node metastases are not seen

neoplasm
increased thyroid carcinoma incidence ( J:208854 )
• mice administered tamoxifen develop papillary thyroid carcinomas
• tumors show both papillary growth morphology and nuclear features of papillary thyroid carcinoma
• even with very long latency, extrathyroidal invasion is not seen and cervical lymph node metastases are not seen

respiratory system
respiratory failure ( J:208854 )
• tamoxifen treated mice generally succumb to respiratory compromise due to tracheal compression by large noninvasive tumors




Genotype
MGI:5897857
cn15
Allelic
Composition		 Braftm1Mmcm/Braf+
Trp53tm3.1Tyj/Trp53+
Tg(TPO-cre/ERT2)1139Tyj/0
Genetic
Background		 involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
Tg(TPO-cre/ERT2)1139Tyj mutation (1 available)
Trp53tm3.1Tyj mutation (2 available); any Trp53 mutation (240 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
mortality/aging
premature death ( J:208854 )
• tamoxifen treated mice exhibit shortened survival

endocrine/exocrine glands
increased thyroid carcinoma incidence ( J:208854 )
• tamoxifen treated mice develop large papillary thyroid carcinoma that exhibit features associated with aggressive behavior including solid growth, tall cell morphology, focal necrosis, and hobnail features
• about 50% of mice with papillary thyroid carcinoma acquire poorly differentiated thyroid carcinoma or undifferentiated anaplastic thyroid carcinoma

neoplasm
increased thyroid carcinoma incidence ( J:208854 )
• tamoxifen treated mice develop large papillary thyroid carcinoma that exhibit features associated with aggressive behavior including solid growth, tall cell morphology, focal necrosis, and hobnail features
• about 50% of mice with papillary thyroid carcinoma acquire poorly differentiated thyroid carcinoma or undifferentiated anaplastic thyroid carcinoma




Genotype
MGI:5897859
cn16
Allelic
Composition		 Braftm1Mmcm/Braf+
Tg(TPO-cre/ERT2)1139Tyj/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background		 involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
Tg(TPO-cre/ERT2)1139Tyj mutation (1 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
mortality/aging
decreased tumor-free survival time ( J:208854 )
• median survival of about 6 months following tumor induction with tamoxifen
• tumor induced mice treated with the BRAF inhibitor PLX4720 show improved survival
• tumor induced mice treated with both the BRAF inhibitor PLX4720 and the selective MEK inhibitor PD0325901show prolonged survival

neoplasm
increased thyroid carcinoma incidence ( J:208854 )
• tamoxifen treated mice exhibit accelerated progression from papillary thyroid carcinoma to poorly differentiated thyroid carcinoma and overt undifferentiated anaplastic thyroid carcinoma with highly pleomorphic, atypical cells with evidence of necrosis
• carcinoma in tamoxifen treated mice shows tracheal invasion and extrathyroidal extension
• marker analysis indicates that anaplastic thyroid carcinoma in tamoxifen treated mice originates from thyroid epithelium
• tumors from tamoxifen treated mice exhibit very slow initial growth upon induction but rapid tumor growth after a variable latency
• mice supplemented with L-thyroxine immediately following tamoxifen administration show suppressed TSH levels and develop anaplastic thyroid carcinoma with a similar latency as unsupplemented controls
• anaplastic thyroid carcinomas exhibit a gene expression profile of high-grade, undifferentiated carcinomas
• tumor induced mice treated with the BRAF inhibitor PLX4720 show improved survival and a decrease in contralateral papillary thyroid carcinomas, however no decrease in anaplastic thyroid carcinoma size is seen and tumors even grow larger
• tumor induced mice treated with both the BRAF inhibitor PLX4720 and the selective MEK inhibitor PD0325901 show complete regression of tumors and prolonged survival
increased metastatic potential ( J:208854 )
• 19% of tamoxifen treated mice exhibit lung metastases
• however, region lymph node metastases are not seen

endocrine/exocrine glands
increased thyroid carcinoma incidence ( J:208854 )
• tamoxifen treated mice exhibit accelerated progression from papillary thyroid carcinoma to poorly differentiated thyroid carcinoma and overt undifferentiated anaplastic thyroid carcinoma with highly pleomorphic, atypical cells with evidence of necrosis
• carcinoma in tamoxifen treated mice shows tracheal invasion and extrathyroidal extension
• marker analysis indicates that anaplastic thyroid carcinoma in tamoxifen treated mice originates from thyroid epithelium
• tumors from tamoxifen treated mice exhibit very slow initial growth upon induction but rapid tumor growth after a variable latency
• mice supplemented with L-thyroxine immediately following tamoxifen administration show suppressed TSH levels and develop anaplastic thyroid carcinoma with a similar latency as unsupplemented controls
• anaplastic thyroid carcinomas exhibit a gene expression profile of high-grade, undifferentiated carcinomas
• tumor induced mice treated with the BRAF inhibitor PLX4720 show improved survival and a decrease in contralateral papillary thyroid carcinomas, however no decrease in anaplastic thyroid carcinoma size is seen and tumors even grow larger
• tumor induced mice treated with both the BRAF inhibitor PLX4720 and the selective MEK inhibitor PD0325901 show complete regression of tumors and prolonged survival

homeostasis/metabolism
increased thyroid-stimulating hormone level ( J:208854 )
• small increase in TSH levels (less than 10-fold elevation) in tamoxifen treated mice
• mice supplemented with L-thyroxine immediately following tamoxifen administration show suppressed TSH levels

respiratory system
respiratory failure ( J:208854 )
• tamoxifen treated mice quickly deteriorate after progression to anaplastic thyroid carcinoma, with rapidly growing neck masses and development of audible respiratory stridor




Genotype
MGI:5902132
cn17
Allelic
Composition		 Braftm1Mmcm/Braf+
Ptentm1Rdp/Ptentm1Rdp
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background		 involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
Ptentm1Rdp mutation (0 available); any Pten mutation (88 available)
Tg(Tyr-cre/ERT2)13Bos mutation (12 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
integument
increased cutaneous melanoma incidence ( J:151023 )
• 7-10 days following 4-hydroxytamoxifen (4-HT) treatment, all mice show expansion of highly pigmented cells that develop into pigmented malignant lesions in locations of 4-HT administration such as the face, flank, or tail skin
• pigmented melanoma cells are seen throughout the dermis and subcutis of 4-HT treated mice and show pagetoid spread into the epidermis
• lesions in 4-HT treated mice progress rapidly to advanced malignancy such that all mice require euthanasia 25-50 days following 4-HT administration
• treatment of 4-HT treated mice with the MEK1/2 inhibitor PD325901 or the mTorc1 inhibitor rapamycin inhibits melanoma formation
• mice in which drug treatment is ceased subsequently develop malignant melanoma
• mice treated once with PD325901 to prevent melanoma remain sensitive to the anti-melanoma action of a second round of PD325901 administration
• treatment of melanoma bearing mice with either PD325901 or rapamycin inhibits further tumor growth but has little or no effect on tumor regression
• treatment of melanoma bearing with both PD325901 or rapamycin results in a 20% reduction in tumor size

neoplasm
increased cutaneous melanoma incidence ( J:151023 )
• 7-10 days following 4-hydroxytamoxifen (4-HT) treatment, all mice show expansion of highly pigmented cells that develop into pigmented malignant lesions in locations of 4-HT administration such as the face, flank, or tail skin
• pigmented melanoma cells are seen throughout the dermis and subcutis of 4-HT treated mice and show pagetoid spread into the epidermis
• lesions in 4-HT treated mice progress rapidly to advanced malignancy such that all mice require euthanasia 25-50 days following 4-HT administration
• treatment of 4-HT treated mice with the MEK1/2 inhibitor PD325901 or the mTorc1 inhibitor rapamycin inhibits melanoma formation
• mice in which drug treatment is ceased subsequently develop malignant melanoma
• mice treated once with PD325901 to prevent melanoma remain sensitive to the anti-melanoma action of a second round of PD325901 administration
• treatment of melanoma bearing mice with either PD325901 or rapamycin inhibits further tumor growth but has little or no effect on tumor regression
• treatment of melanoma bearing with both PD325901 or rapamycin results in a 20% reduction in tumor size
increased metastatic potential ( J:151023 )
• spread of melanoma is seen into the regional draining lymph nodes in 100% of mice and to the lungs in some cases

Mouse Models of Human Disease
 DO ID OMIM ID(s) Ref(s)
skin melanoma DOID:8923 OMIM:608035
OMIM:612263
 J:151023




Genotype
MGI:6192275
cn18
Allelic
Composition		 Braftm1Mmcm/Braftm1Mmcm
Tg(Itgax-cre)1-1Reiz/0
Genetic
Background		 involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
Tg(Itgax-cre)1-1Reiz mutation (4 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
mortality/aging
premature death ( J:211690 )
• decrease in lifespan

immune system
hepatosplenomegaly ( J:211690 )
• severe hepatosplenomegaly
increased dendritic cell number ( J:211690 )
• lesions are associated with massive increase of MHC II+CD11c+ dendritic cells
• expansion of blood circulating dendritic cell precursors and blood circulating dendritic cells
granulomatous inflammation ( J:211690 )
• histiocytic infiltrates in the skin, liver, spleen, and lungs by 8 weeks of age, resulting in a broad destruction of tissue architecture by 16 weeks of age
• histiocytic lesions exhibit classical granulomatous organization, including multinucleated giant cell formation
• granuloma lesions contain massive CD11c+ langerin+ infiltrates, a large number of macrophages, NK cells, B cells, and T cells, with a specific accumulation of regulatory T cells
• local fibrotic response is seen within the granulomas and surrounding stroma
increased inflammatory response ( J:211690 )
• mice rapidly develop an aggressive Langerhans-cells histiocytosis-like disease with 100% penetrance
cytokine storm ( J:211690 )
• granuloma lesions are associated with an increase in several chemokines and cytokines (Ccl2, Ccl15, Il6, Il10, IFN-gamma, and TGF-beta) indicative of a local cytokine storm

hematopoietic system
hepatosplenomegaly ( J:211690 )
• severe hepatosplenomegaly
anemia ( J:211690 )
• severe anemia
increased dendritic cell number ( J:211690 )
• lesions are associated with massive increase of MHC II+CD11c+ dendritic cells
• expansion of blood circulating dendritic cell precursors and blood circulating dendritic cells

growth/size/body
hepatosplenomegaly ( J:211690 )
• severe hepatosplenomegaly

liver/biliary system
hepatosplenomegaly ( J:211690 )
• severe hepatosplenomegaly

Mouse Models of Human Disease
 DO ID OMIM ID(s) Ref(s)
Langerhans-cell histiocytosis DOID:2571 OMIM:246400
OMIM:604856
 J:211690




Genotype
MGI:6393928
cn19
Allelic
Composition		 Braftm1Mmcm/Braf+
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background		 involves: 129P2/OlaHsd * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
Tg(Tyr-cre/ERT2)13Bos mutation (12 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
neoplasm
neoplasm ( J:239472 )
N
• tamoxifen-treated mice do not develop melanoma




Genotype
MGI:3712024
cn20
Allelic
Composition		 Braftm1Mmcm/Braf+
Polr2atm1(cre/ERT2)Bbd/Polr2a+
Genetic
Background		 involves: 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
Polr2atm1(cre/ERT2)Bbd mutation (3 available); any Polr2a mutation (92 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
neoplasm
increased lung adenoma incidence ( J:121715 )
• with induction of Cre expression from the transgene, multiple adenomatous tumors form in mouse lungs

respiratory system
increased lung adenoma incidence ( J:121715 )
• with induction of Cre expression from the transgene, multiple adenomatous tumors form in mouse lungs




Genotype
MGI:5902126
cn21
Allelic
Composition		 Braftm1Mmcm/Braftm1Mmcm
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background		 involves: 129P2/OlaHsd * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
Tg(Tyr-cre/ERT2)13Bos mutation (12 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
pigmentation
abnormal melanocyte morphology ( J:151023 )
• topical administration of 4-hydroxytamoxifen (4-HT) to the ear, tail or flank results in the development of benign melanocytic hyperplasias that are larger and more highly pigmented than in conditional heterozygotes




Genotype
MGI:5902125
cn22
Allelic
Composition		 Braftm1Mmcm/Braf+
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background		 involves: 129P2/OlaHsd * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
Tg(Tyr-cre/ERT2)13Bos mutation (12 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
pigmentation
abnormal melanocyte morphology ( J:151023 )
• pigmented lesions in 4-HT treated mice are frequently located at the dermal-epidermal junction with extension into the dermis, indicating melanocytic nevi
• other melanocytic proliferations form in the dermis with no junctional component in 4-HT treated mice

integument
skin lesions ( J:151023 )
• mice treated with 4-hydroxytamoxifen (4-HT) either topically or systemically develop highly pigmented lesions that are detected by 21-28 days after 4-HT administration; these are small papular pigmented lesions that are not malignant
• topical administration of high concentrations of 4-HT occasionally results in periocular lesions on the face and on the glabrous skin of the paws




Genotype
MGI:5780076
cn23
Allelic
Composition		 Braftm1Mmcm/?
Tg(TPO-cre)1Shk/0
Genetic
Background		 involves: 129P2/OlaHsd * FVB/NCr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
Tg(TPO-cre)1Shk mutation (1 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
growth/size/body
decreased birth weight ( J:172205 )
• mice exhibit low birth weight and fail to thrive




Genotype
MGI:6792072
cn24
Allelic
Composition		 Braftm1Mmcm/Braf+
Gt(ROSA)26Sortm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Tg(Mitf-cre)7114Gsb/0
Genetic
Background		 STOCK Braftm1Mmcm Gt(ROSA)26Sortm14(CAG-tdTomato)Hze Tg(Mitf-cre)7114Gsb/Cvrk
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (60 available)
Gt(ROSA)26Sortm14(CAG-tdTomato)Hze mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Mitf-cre)7114Gsb mutation (0 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cellular
abnormal cell physiology ( J:312561 )
• when cultured on fibronectin-coated plates, inter-follicular epidermis melanocytes exhibit increased survival compared with wild-type mice

integument

limbs/digits/tail

pigmentation




Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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Send questions and comments to User Support. 		last database update
11/12/2024
MGI 6.24 		The Jackson Laboratory