The Administrative Core, led by the Center Director, Dr. Amy S. Paller, and the Associate Center Director, Dr. Robert M. Lavker, will be responsible for coordinating all activities of the SDRC. The Administrative Core will serve as a focal point for all University-wide cutaneous biology-related activities via an Enrichment Program that organizes seminars, workshops, lectures, and one-on-one interactions with distinguished visiting scientists. The Administrative Core will also maintain the SDRC website and disseminate a news letter bi-annually. The Core will continue to encourage investigators to enter the skin biology field through the administration of a Pilot & Feasibility Program that funds four P&F grants per year. At least one P&F grant will be required to focus on a problem that addresses minority or sex issues. The Administrative Core will manage the SDRC laboratory space of the other Research Cores (Skin Tissue Engineering, Morphology and Phenotyping, and DNA/RNA Delivery Core). The Core will also oversee all fiscal maintenance of Center resources including service cost calculations. The Administrative Core will accomplish all of these tasks with guidance from: (i) the SDRC Executive Committee; (ii) an Internal Advisory Board; and (iii) an External Advisory Board. The Core will continue to foster the training of young candidates in the field of skin disease and cutaneous biology through the continued mentorship of the senior SDRC bench research members as well as the Internal and External advisory board members. Finally, through the management of the Minority and Gender Awareness Program, the Administration Core hopes to: (i) promote a better understanding of the biology of all human skin; and (ii) attract and recruit under-represented minorities and women into cutaneous research.
The long-term goal of the SDRC Adminstrative Core will be to continue to coordiante all activities of the Center. Core A facilitates research for all Center members while minimizing user costs and brings together researchers who focus on skin disease and cutaneous biology for exchanges of thought and collaboration.
|Kishibe, Mari; Griffin, Tina M; Goslawski, Melissa et al. (2018) Topical nicotinic receptor activation improves wound bacterial infection outcomes and TLR2-mediated inflammation in diabetic mouse wounds. Wound Repair Regen 26:403-412|
|Kam, Chen Yuan; Dubash, Adi D; Magistrati, Elisa et al. (2018) Desmoplakin maintains gap junctions by inhibiting Ras/MAPK and lysosomal degradation of connexin-43. J Cell Biol 217:3219-3235|
|North, Jeffrey P; Golovato, Justin; Vaske, Charles J et al. (2018) Cell of origin and mutation pattern define three clinically distinct classes of sebaceous carcinoma. Nat Commun 9:1894|
|Rübsam, Matthias; Broussard, Joshua A; Wickström, Sara A et al. (2018) Adherens Junctions and Desmosomes Coordinate Mechanics and Signaling to Orchestrate Tissue Morphogenesis and Function: An Evolutionary Perspective. Cold Spring Harb Perspect Biol 10:|
|Chu, Lan H; Indramohan, Mohanalaxmi; Ratsimandresy, Rojo A et al. (2018) The oxidized phospholipid oxPAPC protects from septic shock by targeting the non-canonical inflammasome in macrophages. Nat Commun 9:996|
|Tsoi, Lam C; Yang, Jingjing; Liang, Yun et al. (2018) Transcriptional determinants of individualized inflammatory responses at anatomically separate sites. J Allergy Clin Immunol 141:805-808|
|Kaplan, Nihal; Ventrella, Rosa; Peng, Han et al. (2018) EphA2/Ephrin-A1 Mediate Corneal Epithelial Cell Compartmentalization via ADAM10 Regulation of EGFR Signaling. Invest Ophthalmol Vis Sci 59:393-406|
|Nekrasova, Oxana; Harmon, Robert M; Broussard, Joshua A et al. (2018) Desmosomal cadherin association with Tctex-1 and cortactin-Arp2/3 drives perijunctional actin polymerization to promote keratinocyte delamination. Nat Commun 9:1053|
|Ratsimandresy, Rojo A; Chu, Lan H; Khare, Sonal et al. (2017) The PYRIN domain-only protein POP2 inhibits inflammasome priming and activation. Nat Commun 8:15556|
|Bagchi, Sreya; He, Ying; Zhang, Hong et al. (2017) CD1b-autoreactive T cells contribute to hyperlipidemia-induced skin inflammation in mice. J Clin Invest 127:2339-2352|
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