The primary objective of the Morphology Core is to enhance the versatility and productivity of both new P&F investigators and established skin investigators by facilitating access to techniques directed at the microscopic analysis of skin samples. This will be accomplished by maintaining banks of proven reagents (antisera), executing immunostaining protocols, screening new antisera, instructing/optimizing in situ hybridization protocols screening transgenic mice for histologic skin abnormalities, and providing dermatopathologic assistance. This core will provide a pioneering/nurturing environment where cutting edge microscopic techniques are initially tried and achieved under the guidance of an experienced team. The core will implement the introduction of new techniques with greater sensitivities and generate clusters of pathway- specific techniques (integrin panels, apoptosis markers, signals transduction probes and antisera) to the greater SDRC user group, and hasten the conversion from isotopic based protocols to non-isotopic methods. The Core will render state-of-the-art embedding, sectioning, staining, quantitative morphometry, photographic layout and printing for microscopic specimens on a timely and low-cost basis. Another prime- function of the Morphology Core will be to procure clinical-derived human samples with accurate demographic and diagnostic data. The continue availability of large, centralized bank of dermatopathologic and wound healing samples is a critical component and invaluable resource for investigators who conduct skin-related projects. The Director and all research assistants will supply teaching assistance and advice in microscopic techniques useful for skin analysis for P&F investigators, Funded SDRC investigators and their post-doctoral fellows, graduate students, and laboratory personnel. Cooperative interactions among the Molecular Genetics and Phenotype Cores will occur on a daily basis snap frozen tissues are delivered to the Molecular Genetics Core or animal samples and/or cultured cells are generated from the Phenotype Core.
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| Velez Edwards, Digna R; Tsosie, Krystal S; Williams, Scott M et al. (2014) Admixture mapping identifies a locus at 15q21.2-22.3 associated with keloid formation in African Americans. Hum Genet 133:1513-23 |
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| Takahashi, Keiko; Mernaugh, Raymond L; Friedman, David B et al. (2012) Thrombospondin-1 acts as a ligand for CD148 tyrosine phosphatase. Proc Natl Acad Sci U S A 109:1985-90 |
| Jandova, Jana; Eshaghian, Alex; Shi, Mingjian et al. (2012) Identification of an mtDNA mutation hot spot in UV-induced mouse skin tumors producing altered cellular biochemistry. J Invest Dermatol 132:421-8 |
| Jandova, Jana; Shi, Mingjian; Norman, Kimberly G et al. (2012) Somatic alterations in mitochondrial DNA produce changes in cell growth and metabolism supporting a tumorigenic phenotype. Biochim Biophys Acta 1822:293-300 |
| Sundberg, J P; Taylor, D; Lorch, G et al. (2011) Primary follicular dystrophy with scarring dermatitis in C57BL/6 mouse substrains resembles central centrifugal cicatricial alopecia in humans. Vet Pathol 48:513-24 |
| Harries, M J; Sun, J; Paus, R et al. (2010) Management of alopecia areata. BMJ 341:c3671 |
| Yang, Jinming; Splittgerber, Ryan; Yull, Fiona E et al. (2010) Conditional ablation of Ikkb inhibits melanoma tumor development in mice. J Clin Invest 120:2563-74 |
| Russell, Shirley B; Russell, James D; Trupin, Kathryn M et al. (2010) Epigenetically altered wound healing in keloid fibroblasts. J Invest Dermatol 130:2489-96 |
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