The primary objective of the Molecular Genetics Core is to provide technical support for both new andestablished investigators by assisting in the design and implementation of molecular biologic techniques focusedon identifying and characterizing novel regulatory and structural skin associated genes. The Core has and willcontinue to isolate nucleic acids from tissues and cell cultures for further genetic analyses. In addition, it servesto assist in the design, construction, and production of classic expression and Adenoviral, and Adeno-associatedviral vectors to examine the functional properties of those genes deemed of interest. All of these techniques andanalyses are and will be provided in a timely fashion on a reasonable per service fee basis. Not only will the Coreprovide technical support, but the directors and research assistant will supply teaching assistance and directionwhen solicited by all investigators of the Vanderbilt research community, with preference given to SDRCinvestigators, including P & F investigators, their post-doctoral fellows, graduate students, and laboratorypersonnel. The Core will continue to implement the introduction of new technologies to enhance the caliber ofdata obtained through interactions with the Core. For example, over the past funding period the Core has finetunedthe production, isolation and purification of Adeno-associated viral vectors (AAV2) in conjunction with thePhenotype Core of the SDRC. In addition the Core has secured a large contract project in conjunction with theVanderbilt Microarray Shared Resource that will provide significant program income during year 15. During thelifetime of the Vanderbilt SDRC, such cooperative interactions have increased to provide a complete pipelinefrom which investigators may identify a gene of interest, examine this gene both in vitro and in vivo utilizinghistologic and molecular techniques, and generate expression vectors to more rigorously examine this gene anddetermine the functional consequence of its expression to specific skin-related disease processes.
| Russell, Shirley B; Smith, Joan C; Huang, Minjun et al. (2015) Pleiotropic Effects of Immune Responses Explain Variation in the Prevalence of Fibroproliferative Diseases. PLoS Genet 11:e1005568 |
| 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 |
| Duncan, F Jason; Silva, Kathleen A; Johnson, Charles J et al. (2013) Endogenous retinoids in the pathogenesis of alopecia areata. J Invest Dermatol 133:334-43 |
| 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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