Search Criteria: Research Area is "Dermatology Research: Other"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 013787 | B6.129S1-Abcc6tm1Jfk/J | Repository- Live |
| Mice that are homozygous for this targeted mutation develop patchy, progressive mineralization of the dermis, kidneys, eyes, arteries, heart and subcutaneous tissues, mimicking the human disease symptoms of pseudoxanthoma elasticum. Mineralization of connective tissue capsule surrounding vibrissae is detectable at 5 weeks of age. Mineralization is associated with collagen fibrils and elastic fibers. Oxidative stress, as indicated by lipid peroxidation and protein oxidation, is higher in liver tissue and serum of mutant mice when compared to wildtype controls. Antioxidant diet reduces the oxidative stress levels in knock out mice, but does not prevent ectopic mineralization. The severity of mineralization can be altered by mineral intake as a diet with elevated magnesium levels prevents pathological connective tissue mineralization in mutants. Serum matrix gla protein (MGP) levels are reduced in homozygotes and the protein is under-carboxylated with diminished activity. Fetuin-A ..... For more information please see the full phenotype on the strain data sheet | ||
| 012564 | B6.129S5-Dhcr24tm1Fein/SbpaJ | Repository- Live |
| Homozygous mice on the C57BL/6 genetic background die within the first postnatal day with features of lethal restrictive dermopathy; including taut, wrinkle-free, shiny skin, severe defects in epidermal maturation/epidermal barrier function (impaired epidermal development), and increased presence of hyperproliferative immature keratinocytes (defective keratinocyte differentiation). The increased transepidermal water loss/increased epidermal water content is associated with increased aquaporin-3 (AQP3) expression throughout the epidermis. Mice heterozygous for this allele are viable and fertile, with no overt phenotype. As the Dhcr24 protein functions to catalyze the last step of cholesterol biosynthesis (the conversion of desmosterol to cholesterol), homozygous disruption of this locus results in desmosterolosis: almost no cholesterol in plasma and tissues with ~99% of total sterols in the form of desmosterol. lacZ expression from the mutant allele is not characterized.
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| 013193 | B6;129S-Barhl1tm1Xia/J | Repository- Live |
| In this strain, the entire coding region of the endogenous BarH-like 1 (Barhl1) gene is replaced with a lacZ (β-galactosidase) reporter gene and a loxP-flanked neomycin resistance (neo) cassette, abolishing gene function. Homozygous mice are viable, fertile, and normal in size, with β-gal staining in Barhl1 expressing tissues. LacZ expression in embryos and neonates is evident in all hair cells, but is more abundantly observed in the cochlear outer hair cells. LacZ expression in adults is strong in the outer hair cells, and weak in the inner and vestibular hair cells, with persistent expression in hair cells of the organ of Corti. These mice exhibit age-related progressive degeneration of both cochlear outer and cochlear inner hair cells in the organ of Corti, resulting in hearing loss. The progression is apical-to-basal for outer hair cell and basal-to-apical for inner hair cells. Barhl1-/- mice have elevated audit ..... For more information please see the full phenotype on the strain data sheet | ||
| 005440 | C.129S4-Ccr3tm1Cge/J | Repository- Live |
| Mice homozygous for this CCR3 (chemokine (C-C motif) receptor 3) targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RNA protection assay analysis of thymus, spleen and lung tissues. Mice homozygous for the mutation have impaired trafficking of eosinophils. A 7-fold decrease in the number of eosinophils in the small intestine and a 6-fold increase in the spleen is observed. Aerosol allergen challenge does not cause the expected infiltration of eosinophils to the lung tissue and airway lumens (50-70% reduction), although abundant eosinophils are found in the airway blood vessels. Concurrent increases in eosinophils in the spleen and intraepithelial mast cells in the spleen occur after allergen challenge. Homozygotes exhibit increased bronchoconstriction with allergen-induced airway hyperresponsiveness. There is no increase in eosinophils or eosinophil product major basic protein (M ..... For more information please see the full phenotype on the strain data sheet | ||
| 012874 | STOCK Map3k11m1J/GrsrJ | Repository- Live |
| Mice homozygous for the Map3k11m1J mutation can be identified easily as early as 3 to 4 days of age by the dorsal lines of dark red skin that run from head to tail along the spine and from left to right across the crown of the head, base of the neck in front of the shoulders, and between the base of the ribs and the pelvis. These lines fade away and by 3 weeks of age are no longer evident even when the homozygote is shaved to expose the skin. Homozygotes have necrotic dental pulp, which also improves with age. | ||
| 004623 | STOCK Tg(Fos-lacZ)34Efu/J | Repository- Live |
| These TOPGAL transgenic mice are a reporter strain that express Beta-galactosidase in the presence of the lymphoid enhancer binding factor 1/transcription factor 3 (LEF/TCF) mediated signaling pathway and activated Beta-catenin. The transgene contains the lacZ gene under the control of a regulatory sequence consisting of three consensus LEF/TCF-binding motifs upstream of a minimal c-fos promoter. Transgenic mice display TOPGAL activity (Beta-galactosidase activity) during early embryonic development in a subset of pluripotent embryonic basal cells of the epithelium and dermis of developing hair follicles, but not during the next stage of hair follicle development; formation of hair germs. TOPGAL transgene activity reappears in hair follicles at E16.5 and TOPGAL expression is strongly upregulated in the postnatal hair shaft precursor cells in both whisker and body hair anagen follicles (active periods of hair growth). TOPGAL expression ceases during catagen (regression and ..... For more information please see the full phenotype on the strain data sheet | ||
| 005107 | STOCK Tg(KRT14-cre/ERT)20Efu/J | Repository- Live |
| These transgenic mice have a tamoxifen inducible Cre-mediated recombination system driven by the human keratin 14 (KRT14) promoter. The transgene insert contains a fusion product involving Cre recombinase and a mutant form of the mouse estrogen receptor ligand binding domain. The mutant mouse estrogen receptor does not bind natural ligand at physiological concentrations but will bind the synthetic ligand, 4-hydroxytamoxifen (tamoxifen). Restricted to the cytoplasm, the cre/Esr1 protein can only gain access to the nuclear compartment after exposure to tamoxifen. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted keratinocyte-specific deletions. Oral tamoxifen administration induces Cre recombination in toe, back skin and tongue. Topically administered tamoxifen induces Cre-mediated recombination in a specific localized area of the skin, occuring in 50 to 60% of the ..... For more information please see the full phenotype on the strain data sheet | ||
| 006403 | 129S.B6-Tg(KRT14-Esr1/HRAS)1Pkha/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this "K14-ER:Ras" transgene are viable and fertile, with expression of the ER:Ras fusion protein (constitutively active G12V mutant form of the catalytic domain of human H-ras (H-rasV12) fused at its amino terminal with the G525R mutant murine estrogen receptor ligand binding domain (ERTM)) directed to epidermis by the human keratin 14 promoter. Because of the ERTM region of the fusion protein, ER:Ras is restricted to the cytoplasm and the biochemical activity of the ER:Ras fusion gene can be induced following tamoxifen administration. For example, prolonged (4 weeks) induction of human H-RasG12V activity promotes the undifferentiated, proliferative phenotypic characteristics observed in epidermal cancer; including hyperplasia, increased mitotic index, decreased expression of differentiation markers and increased expression of beta-1 and beta-4 integrin subunits. H-RasG12V-induced skin abnormalities were entirely reversed ..... For more information please see the full phenotype on the strain data sheet | ||
| 006661 | 129S.B6-Tg(KRT14-RAF1/ESR1)1Pkha/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this "K14-Raf:ER" transgene are viable and fertile, with expression of the Raf:ER fusion protein (a constitutively active Y340D/Y341D mutant form of the catalytic domain of human Raf-1 (Raf-1[DD]) fused at its carboxy terminal with the G525R mutant human estrogen receptor ligand binding domain (ERTM)) directed to epidermis by the human keratin 14 promoter. Because of the ERTM region of the fusion protein, Raf:ER is restricted to the cytoplasm and the biochemical activity of the Raf:ER fusion gene can be induced following tamoxifen administration. For example, prolonged (4 weeks) induction of human Raf-1[DD] activity promotes the undifferentiated, proliferative phenotypic characteristics observed in epidermal cancer; including hyperplasia, increased mitotic index, decreased expression of differentiation markers and increased expression of beta-1 and beta-4 integrin subunits. Raf-1[DD]-induced skin abnormalities are entirely reversed within one m ..... For more information please see the full phenotype on the strain data sheet | ||
| 006201 | B6.129-Scd1tm1Ntam/J | Cryopreserved - Ready for recovery |
| Homozygous mice are viable and fertile. Transcripts from the targeted gene are absent in homozygous liver, eyelid, skin, and white adipose tissues. In addition, the endogenous protein and enzyme activity are absent from homozygous liver tissue. Homozygous mice exhibit cutaneous abnormalities and narrow eye fissure with atrophic sebaceous and meibomian glands. Mutant mice also have reduced body adiposity, increased insulin sensitivity, increased basal and insulin-mediated glucose uptake, and are resistant to diet-induced weight gain. Homozygotes have altered hepatic glycerophospholipid profiles. Homozygous mice are not recommended for breeding as skin lesion severity may prohibit colony success. These mutant mice may be useful in studies of monounsaturated fatty acid synthesis, cholesterol homeostasis, skin disease, obesity, and diabetes. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background differ ..... | ||
| 006879 | B6.129-Scd2tm1Myz/J | Cryopreserved - Ready for recovery |
| While heterozygous mice are viable and fertile, mice homozygous for this targeted allele die within 24 hours of birth. Brain tissues from homozygous mice show no expression from the targeted gene. Homozygotes exhibit neonatal lethality with 100% penetrance on this genetic background (less penetrant on 129SvEv genetic background) likely due to severe skin permeability barrier abnormalities. Null mice also have abnormal epidermal morphology and abnormal lipid homeostasis in the skin and liver. These mutant mice may be useful in studying monounsaturated fatty acid synthesis, lipid biosynthesis and metabolism, cholesterol homeostasis, and skin disease, as well as obesity and diabetes. | ||
| 007015 | B6.129S1-Gadd45gtm1Flv/J | Cryopreserved - Ready for recovery |
| Homozygotes are viable and fertile, but are poor breeders. TH1 helper T cells from homozygotes are severely compromised in their abilities to activate p38 (MAPK14)and JNK (MAPK8) in response to T cell receptor (TCR) signaling, produce much less interferon gamma (IFNG) upon restimulation, and are deficient in activation-induced cell death (AICD). Deficiencies in this gene also cause reduced contact hypersensitivity in the animals. | ||
| 004042 | B6.129S2-Alox12tm1Fun/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for the Alox12 gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Alox12 protein product or enzyme activity is detected in platelets derived from homozygous null animals. Platelets exhibit a hyperresponsiveness to ADP-induced aggregation. Studies examining basal transepidermal water loss indicate that null animals exhibit greater water loss through the skin when compared to control animals. | ||
| 009687 | B6.Cg-Tg(KRT14-Kitl*)4XTG2Bjl/J | Cryopreserved - Ready for recovery |
| These transgenic mice express a mutant mouse Kitl (kit ligand) cDNA, TG2 or membrane SCF, under the control of the human keratin 14 (epidermolysis bullosa simplex, Dowling-Meara, Koebner), KRT14, promoter. The mutant kit ligand carries a site directed mutation that deletes the cleavage site which produces mostly membrane bound protein. These transgenic mice have epidermal melanocytes that persist into adulthood and cause grey-black pigmented skin and increased coat pigment. Shortly after birth, transgenic pups develop visibly pigmented footpads. Transgenic mice exhibit increased sensitivity to irritants. Mice that are homozygous for the targeted mutation are viable, and do not display any gross behavioral abnormalities. Homozygotes are sometimes smaller in size than wildtype controls (as reported by the Donating Investigator). This mutant mouse strain may be useful in studies of hyperpigmentation and allergic contact dermatitis. | ||
| 007678 | B6;SJL-Tg(KRT14-rtTA)208Jek/J | Cryopreserved - Ready for recovery |
| Homozygous females and hemizygous males carrying this X-linked K14-rtTA transgene (K14-rtTetA(X) or rtTAX) are viable and fertile. These mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the human keratin 14 promoter. As the transgene is located on the X chromosome, random inactivation of the X chromosome may result in mosaic rtTA expression patterns in female mice. When mated to a second transgenic strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE or tetO), expression of the target gene in the basal cells of the squamous epithelia and in the outer root sheath of the hair follicles is induced with administration of the tetracycline analog, doxycycline (dox). These K14-rtTA mice provide a Tet-On tool that allows the inducible expression of genes in skin cells. | ||
| 002662 | C.Cg-Fechm1Pas/J | Cryopreserved - Ready for recovery |
| Homozygous mutants are recognizable by the intense yellow color of their sera, gross bilirubinemia, and, especially in albino mice, jaundice. Photosensitivity is evidenced by the appearance of inflammatory skin lesions, often becoming ulcerous, under standard mouseroom conditions (fluorescent light). Mutants do not differ from their normal littermates in body size or weight, nor are they retarded in growth. They exhibit hepatomegaly and splenomegaly, leading to enlarged abdomens after several months of age. Although mutants are not anemic at one month old, normocytic anemia develops with age. | ||
| 006822 | FVB-Tg(KRT14-MAP2K1/Esr1)12Pkha/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this "K14-Mek1:ER" transgene are viable and fertile, with expression of the Mek1:ER fusion protein (a constitutively active mutant region from human mitogen activated protein kinase-kinase 1 (Mek1R4F; containing an amino-terminal deletion of aa 32-51 and the S218E/S222D substitutions) fused at its carboxy terminal with the G525R mutant murine estrogen receptor ligand binding domain (ERTM)) directed to epidermis by the human keratin 14 promoter. Because of the ERTM region of the fusion protein, Mek1:ER is restricted to the cytoplasm and the biochemical activity of the Mek1:ER fusion gene can be induced following tamoxifen administration. For example, induction of this constitutively active form of human Map2k1 (Mek1R4F) promotes the undifferentiated, proliferative phenotypic characteristics observed in epidermal neoplasia in as few as 5 days (including hyperplasia, increased levels of phosphorylated ERK1/2, increased mitot ..... For more information please see the full phenotype on the strain data sheet | ||
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