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Allele Symbol Allele Name Allele ID |
Braftm1Cpri targeted mutation 1, Catrin Pritchard MGI:3612533 |
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| Summary |
12 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• serum starved and replete recombined mouse embryonic fibroblasts (MEFs) display increased proliferation with 9.57% and 26.2% of cells entering S-phase, respectively, compared to 6.75% and 11.5% for starved and fed wild-type cells, respectively
• recombined MEFs can also grow at higher densities and lose contact inhibition
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice infected with adenovirus cre exhibit increased incidence of lung tumors compared with Krastm4Tyj heterozygotes
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• in mice infected with adenovirus cre
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• primary mouse embryonic fibroblast treated with adenoviral-cre exhibit enhanced growth rate compared with wild-type cells
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• mice infected with adenovirus cre exhibit increased incidence of lung tumors compared with Krastm4Tyj heterozygotes
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• in mice infected with adenovirus cre
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• behavioral responses to pain and motor functions are similar to controls prior to the onset of scratching
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• at 4 to 6 weeks of age, show enhanced scratching responses to pruritogens injected into the nape
• both histaminergic and nonhistaminergic itch are significantly enhanced
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• age-dependent excessive scratching from 6 to 14 weeks of age, with about 50% of mice showing excessive scratching at 6 weeks of age
• at 4 to 6 weeks of age, show enhanced scratching responses to pruritogens injected into the nape
• both histaminergic and nonhistaminergic itch are significantly enhanced
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• develop after the onset of excessive scratching
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• increase in the density of primary afferent fibers innervating the cervical and lumbar back hairy skin regions
• in the spinal cord CGRP+ fibers expand into lamina II inner layer and nonpeptidergic
• IB4+ fibers invade into laminae I and II outer layer domains
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• increase in the number of pERK+ cells in dorsal root ganglion neurons at the cervical, thoracic and lumbar segmental levels
• the number of GRP+ neurons is nearly doubled
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• the percentage of single spike cells is decreased while the percentage of delayed firing cells is almost
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• increase in the percentage of dorsal root ganglion cells responding to chloroquine and histamine
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• spontaneous scratching, seen in mutant mice wild-type for Grpr, is markedly diminished
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• spontaneous scratching, seen in mutant mice wild-type for Grp, is markedly diminished
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• architecture of thyroid follicles is disrupted at 3 weeks of age
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• mice develop low-grade papillary thyroid cancer by 9 weeks of age, however, tumors are smaller and lack the characteristic tall cell features and are less invasive than in single Braftm1Cpri conditional mice
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• mice develop low-grade papillary thyroid cancer by 9 weeks of age, however, tumors are smaller and lack the characteristic tall cell features and are less invasive than in single Braftm1Cpri conditional mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice develop smaller papillary thyroid tumors with greatly attenuated histological features resembling indolent papillary thyroid cancer in humans compared to single Braftm1Cpri conditional mutants
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• mice develop smaller papillary thyroid tumors with greatly attenuated histological features resembling indolent papillary thyroid cancer in humans compared to single Braftm1Cpri conditional mutants
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• embryos with high levels of Cre mediated recombination are in the process of being resorbed at E7.5, while those with more mosaic recombination survived to later ages but still die before birth
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• even in the absence of pI-pC injection to induce Cre expression some recombination is seen and all mice are dead before 4 weeks of age
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• histiocytes containing the recombined allele are found in extranodal sites predominantly in the skin consistent with nonlymphoid leukemia of the histiocytic type
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• seen in the spleen and liver
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• red and white blood cell numbers in the bone marrow are reduced with red blood cells virtually absent
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• increased proliferation and apoptosis are seen
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• tamoxifen-treated mice develop nevi most commonly at the site of application with some large melanocytic lesions around the perianal regions and in the eyelids unlike in control mice (either treated with only ethanol or lacking one of the alleles)
• nevi in tamoxifen-treated mice are slowly proliferating, dome-shaped outgrowths in the dermis composed of pigmented epithelioid or dendritic melanocytes with neuroid differentiation in some cases
• 80% of tamoxifen-treated mice develop eyelid nevi 3 to 5 months after treatment
• mice treated with high doses of tamoxifen develop perianal nevi 6 to 10 months after treatment
• 60% to 70% of tamoxifen-treated mice develop rapidly growing, invasive hypopigmented skin tumors that often (in 38% of mice) ulcerate the overlying epidermis, infiltrate the subcutis, skeletal muscle, and auricular cartilage and display characteristics of malignant melanomas
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• some tamoxifen-treated mice develop oligomelanotic malignant melanomas unlike control mice (either treated with only ethanol or lacking one of the alleles)
• 54% of tamoxifen-treated mice develop melanomas within 12 months
• 64% of tamoxifen-treated mice develop melanomas after 14 months
• median latency to develop melanomas in a tamoxifen-treated mouse is 12 months
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• following application of tamoxifen on the back, snouts, tails, ears, and paws are visibly darkened compared to in control mice (either treated with only ethanol or lacking one of the alleles)
• following application of tamoxifen on the back, 40% of mice develop darkened toenails proximal to the body on the front or hind feet unlike control mice
• following application of tamoxifen on the back, 50% of females develop darkened nipples unlike control mice
• following application of tamoxifen on the back, hairy skin is darkened most noticeable at the site of application unlike control mice
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• in 38% of tamoxifen-treated mice
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• tamoxifen-treated mice develop nevi most commonly at the site of application with some large melanocytic lesions around the perianal regions and in the eyelids unlike in control mice (either treated with only ethanol or lacking one of the alleles)
• nevi in tamoxifen-treated mice are slowly proliferating, dome-shaped outgrowths in the dermis composed of pigmented epithelioid or dendritic melanocytes with neuroid differentiation in some cases
• 80% of tamoxifen-treated mice develop eyelid nevi 3 to 5 months after treatment
• mice treated with high doses of tamoxifen develop perianal nevi 6 to 10 months after treatment
• 60% to 70% of tamoxifen-treated mice develop rapidly growing, invasive hypopigmented skin tumors that often (in 38% of mice) ulcerate the overlying epidermis, infiltrate the subcutis, skeletal muscle, and auricular cartilage and display characteristics of malignant melanomas
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice weigh about 50% less than wild-type littermates by weaning
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• by 5 weeks of age, serum TSH levels are about 500-fold greater than in wild-type mice
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• by 5 weeks of age, serum T4 levels are decreased
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• mice develop infiltrative papillary thyroid cancer with complete penetrance by 5 weeks of age
• tumors encompass the entire thyroid gland and have features of aggressive human papillary thyroid cancer with papillae lined by tall cells, with increased number of mitoses, nuclear clearing, and pseudonuclear inclusions
• administration of levothyroxine (L-T4) soon after birth for 3 weeks does not prevent the onset or alter the characteristics of papillary thyroid tumors
• administration of L-T4 for 3 weeks beginning at 5 weeks of age when all mice have tumors does not decrease the mitotic rate or alter the severity of the tumors
• mice treated with the MEK1/2 inhibitor PD325901 for 3 weeks beginning at 3 weeks of age exhibit a decrease in thyroid tumor volume and a modest reduction in proliferative index of tumors
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• tumor cells frequently invade perithyroidal tissues
• 66% of tumors invade into surrounding skeletal muscle by 5 weeks and vascular invasion is common
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• mice develop infiltrative papillary thyroid cancer with complete penetrance by 5 weeks of age
• tumors encompass the entire thyroid gland and have features of aggressive human papillary thyroid cancer with papillae lined by tall cells, with increased number of mitoses, nuclear clearing, and pseudonuclear inclusions
• administration of levothyroxine (L-T4) soon after birth for 3 weeks does not prevent the onset or alter the characteristics of papillary thyroid tumors
• administration of L-T4 for 3 weeks beginning at 5 weeks of age when all mice have tumors does not decrease the mitotic rate or alter the severity of the tumors
• mice treated with the MEK1/2 inhibitor PD325901 for 3 weeks beginning at 3 weeks of age exhibit a decrease in thyroid tumor volume and a modest reduction in proliferative index of tumors
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• tumor cells frequently invade perithyroidal tissues
• 66% of tumors invade into surrounding skeletal muscle by 5 weeks and vascular invasion is common
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• mice are euthyroid at P3, however by 5 weeks of age, mice are hypothyroid
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| thyroid gland papillary carcinoma | DOID:3969 |
OMIM:188550 |
J:168249 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• tamoxifen-treated mice develop multiple tumors unlike Braftm1Cpri/Braftm1Cpri Tg(Tyr-cre/ERT2)1Laru mice that develop single tumors
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• tamoxifen-treated mice develop nevi unlike control mice (either treated with only ethanol or lacking one of the alleles)
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• 80% of tamoxifen-treated mice develop melanomas within 12 months
• median latency to develop melanomas in a tamoxifen-treated mouse is 7 months
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• tamoxifen-treated mice develop nevi unlike control mice (either treated with only ethanol or lacking one of the alleles)
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• tamoxifen-treated mice develop multiple tumors unlike Braftm1Cpri/Braftm1Cpri Tg(Tyr-cre/ERT2)1Laru mice that develop single tumors
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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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last database update 04/09/2024 MGI 6.23 |
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