Faculty

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Wei Li, PhD
Professor of Dermatology
Director, Mss Graduate Program
Dermatology
NOR 5301 1441 Eastlake Avenue Health Sciences Campus Los Angeles
+1 323 865 0618

Overview

Dr. Li research focuses on the following topics: 1) Identification of the "driver genes" for wound healing, 2) Identification of tumor-secreted molecules as drug targets for TNBCs (triple negative breast cancers). 3) Signal transduction to understand the cell motility signaling, which initiates at the cell surface, propagates via cytosolic signaling networks and executes by newly expressed and secreted gene products.

His experimental model systems are less manipulated primary human skin cells, whose migration is essential for both physiological processes, such as skin wound healing, and pathological occurrence, such as skin cancer, PDX models for TNBCs and pig models for wound healing.

Publications

Evolutionarily conserved dual lysine motif determines the non-chaperone function of secreted Hsp90alpha in tumour progression. Oncogene. 2017 Apr; 36(15):2160-2171. View in: PubMed

Evolutionarily conserved dual lysine motif determines the non-chaperone function of secreted Hsp90alpha in tumour progression. Oncogene. 2016 Oct 10. View in: PubMed

Keratinocyte-Secreted Heat Shock Protein-90alpha: Leading Wound Reepithelialization and Closure. Adv Wound Care (New Rochelle). 2016 Apr 01; 5(4):176-184. View in: PubMed

Breast Cancer MDA-MB-231 Cells Use Secreted Heat Shock Protein-90alpha (Hsp90a) to Survive a Hostile Hypoxic Environment. Sci Rep. 2016 Feb 05; 6:20605. View in: PubMed

Breast Cancer MDA-MB-231 Cells Use Secreted Heat Shock Protein-90alpha (Hsp90a) to Survive a Hostile Hypoxic Environment. Sci Rep. 2016; 6:20605. View in: PubMed

Hsp90a and Hsp90ß together operate a hypoxia and nutrient paucity stress-response mechanism during wound healing. J Cell Sci. 2015 Apr 15; 128(8):1475-80. View in: PubMed

Influence of the stiffness of three-dimensional alginate/collagen-I interpenetrating networks on fibroblast biology. Biomaterials. 2014 Oct; 35(32):8927-36. View in: PubMed

Identification of the critical therapeutic entity in secreted Hsp90a that promotes wound healing in newly re-standardized healthy and diabetic pig models. PLoS One. 2014; 9(12):e113956. View in: PubMed

Extracellular heat shock protein 90 signals through subdomain II and the NPVY motif of LRP-1 receptor to Akt1 and Akt2: a circuit essential for promoting skin cell migration in vitro and wound healing in vivo. Mol Cell Biol. 2013 Dec; 33(24):4947-59. View in: PubMed

Extracellular Hsp90 (eHsp90) as the actual target in clinical trials: intentionally or unintentionally. Int Rev Cell Mol Biol. 2013; 303:203-35. View in: PubMed

The anti-motility signaling mechanism of TGFß3 that controls cell traffic during skin wound healing. Biol Open. 2012 Dec 15; 1(12):1169-77. View in: PubMed

Secreted heat shock protein-90 (Hsp90) in wound healing and cancer. Biochim Biophys Acta. 2012 Mar; 1823(3):730-41. View in: PubMed

A potentially common peptide target in secreted heat shock protein-90a for hypoxia-inducible factor-1a-positive tumors. Mol Biol Cell. 2012 Feb; 23(4):602-13. View in: PubMed

A fragment of secreted Hsp90a carries properties that enable it to accelerate effectively both acute and diabetic wound healing in mice. J Clin Invest. 2011 Nov; 121(11):4348-61. View in: PubMed

A fragment of secreted Hsp90a carries properties that enable it to accelerate effectively both acute and diabetic wound healing in mice. J Clin Invest. 2011 Nov 1; 121(11):4348-61. View in: PubMed

TbetaRI/Alk5-independent TbetaRII signaling to ERK1/2 in human skin cells according to distinct levels of TbetaRII expression. J Cell Sci. 2011 Jan 1; 124(Pt 1):19-24. View in: PubMed

TbetaRI/Alk5-independent TbetaRII signaling to ERK1/2 in human skin cells according to distinct levels of TbetaRII expression. J Cell Sci. 2011 Jan 01; 124(Pt 1):19-24. View in: PubMed

Participation of the lipoprotein receptor LRP1 in hypoxia-HSP90alpha autocrine signaling to promote keratinocyte migration. J Cell Sci. 2009 May 15; 122(Pt 10):1495-8. View in: PubMed

Characterization of molecular mechanisms underlying mutations in dystrophic epidermolysis bullosa using site-directed mutagenesis. J Biol Chem. 2008 Jun 27; 283(26):17838-45. View in: PubMed

Transforming growth factor alpha (TGFalpha)-stimulated secretion of HSP90alpha: using the receptor LRP-1/CD91 to promote human skin cell migration against a TGFbeta-rich environment during wound healing. Mol Cell Biol. 2008 May; 28(10):3344-58. View in: PubMed

Extracellular heat shock protein-90alpha: linking hypoxia to skin cell motility and wound healing. EMBO J. 2007 Mar 7; 26(5):1221-33. View in: PubMed

Extracellular heat shock protein-90alpha: linking hypoxia to skin cell motility and wound healing. EMBO J. 2007 Mar 07; 26(5):1221-33. View in: PubMed

Intravenously injected human fibroblasts home to skin wounds, deliver type VII collagen, and promote wound healing. Mol Ther. 2007 Mar; 15(3):628-35. View in: PubMed

A "traffic control" role for TGFbeta3: orchestrating dermal and epidermal cell motility during wound healing. J Cell Biol. 2006 Mar 27; 172(7):1093-105. View in: PubMed

Injection of recombinant human type VII collagen restores collagen function in dystrophic epidermolysis bullosa. Nat Med. 2004 Jul; 10(7):693-5. View in: PubMed

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