alexa Editor - Paul J. Higgins | The Albany Medical College | 6197
ISSN: 2168-9296

Cell & Developmental Biology
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Paul J. Higgins

Paul J. Higgins Paul J. Higgins
Professor and Center Director
Center for Cell Biology and Cancer Research
Albany Medical College
Albany,New York

Paul J. Higgins received his Ph.D. degree in molecular biology from New York University in 1976. He joined the faculty of the Memorial Sloan-Kettering Cancer Center and the Cornell University School of Medicine in 1977, where he was a member of the program on cell biology/genetics and the program on molecular biology/virology. Dr. Higgins is currently a Professor and Director of the Center for Cell Biology and Cancer Research at the Albany Medical College in Albany, New York. He was the founding Vice President of the Albany Research Institute and currently serves on the Board of Directors. He has been the Chairman of National Institutes of Health and Department of Defense Review Panels, and received several prestigious awards including the Moyer Award and, most recently, the 2008 Excellence Award in Molecular Medicine. Dr. Higgins has been a member of several journal editorial boards, edited books on cancer biology, and published more than 200 peer-reviewed scientific papers.

Research Interest

Our research focuses on the molecular mechanisms underlying transcriptional regulation of the critical inflammation and fibrosis-promoting factor PAI-1 (plasminogen activator inhibitor-1; SERPINE1).  PAI-1 is a major effector of human fibrotic disease where it promotes the development of, and maintains, the inflammatory and angiogenic responses. Our group was the first to establish cell cycle transcriptional controls on the human PAI-1 gene, and the promoter sequences involved, and related these findings to mapping individual growth factor-responsive promoter elements. We also made major advances in defining the signaling cascade that impact PAI-1 transcription in human epithelial cells and discovered a new pathway of cross-talk between two classes of growth factor receptors (EGFR and TGF-R) in PAI-1 expression control.  Our current efforts focus on creation of molecular genetic "reagents", including PAI-1 oligonucleotide decoys, antisense constructs, silencing RNAs and microRNAs that target PAI-1 gene expression in the fibrotic stroma as well as in angiogenic endothelial cells. The molecular basis of PAI-1 transcription and the role of PAI-1 as a pro-survival factor and critical element in angiogenesis are, in fact, the focus of my long-running NIH-funded R01 grant.  Additional studies in my laboratory have implicated the EGFR as a signaling intermediate in the TGF- pathway. We established the mechanism for receptor cross-talk and published a series of papers detailing the trans-activation of the EGFR by TGF- through a pathway involving the signaling intermediates pp60c-src, caveolin-1, and the RhoA GTPase. In this highly-interactive network, TGF- stimulates pp60c-src to phosphorylate the EGFR leading to ERK-dependent phosphorylation of the transcription factor USF2 activating its target gene PAI-1; in the second arm of the cascade, TGF- activation of Rho-ROCK signaling via caveolin-1 down-regulates the Smad phosphatase PPM1A to maintain Smad-dependent co-activation of the PAI-1 gene. Collectively, these events are required to maintain PAI-1 expression in human epithelial and microvessel endothelial cells.



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