M
Michael B. Sporn
Researcher at Dartmouth College
Publications - 561
Citations - 96644
Michael B. Sporn is an academic researcher from Dartmouth College. The author has contributed to research in topics: Transforming growth factor & Transforming growth factor beta. The author has an hindex of 157, co-authored 559 publications receiving 94605 citations. Previous affiliations of Michael B. Sporn include Cornell University & Reata Pharmaceuticals.
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Journal ArticleDOI
Genetic versus chemoprotective activation of Nrf2 signaling: overlapping yet distinct gene expression profiles between Keap1 knockout and triterpenoid-treated mice
Melinda S. Yates,Quynh T. Tran,Patrick M. Dolan,William O. Osburn,Soona Shin,Colin Craig McCulloch,Jay B. Silkworth,Keiko Taguchi,Masayuki Yamamoto,Charlotte R. Williams,Karen T. Liby,Michael B. Sporn,Thomas R. Sutter,Thomas W. Kensler +13 more
TL;DR: Analysis of pharmacologic activation suggests that Nrf2 is the primary mediator of CDDO-Im activity, though other cell-signaling targets are also modulated following an oral dose of 30 micromol/kg.
Journal ArticleDOI
13-cis-retinoic acid: inhibition of bladder carcinogenesis in the rat.
Michael B. Sporn,Robert A. Squire,Charles C. Brown,Joseph M. Smith,Martin L. Wenk,Stephen Springer +5 more
TL;DR: Feeding of the synthetic retinoid, 13-Cis-retinoid acid, inhibited the incidence and extent of bladder cancer in these rats, even when 13-cis- retinoic acid administration was begun after completion of the carcinogen treatment.
Journal ArticleDOI
Design and synthesis of 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid, a novel and highly active inhibitor of nitric oxide production in mouse macrophages
Tadashi Honda,Barbie Ann V. Rounds,Gordon W. Gribble,Nanjoo Suh,Yongping Wang,Michael B. Sporn +5 more
TL;DR: 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid (CDDO) was 400 times more potent than previous compounds made as an inhibitor of production of nitric oxide induced by interferon-gamma in mouse macrophages.
Journal ArticleDOI
TGF-β1 Prevents Hypertrophy of Epiphyseal Chondrocytes: Regulation of Gene Expression for Cartilage Matrix Proteins and Metalloproteases
R. Tracy Ballock,Ahlke Heydemann,Lalage M. Wakefield,Kathleen C. Flanders,Anita B. Roberts,Michael B. Sporn +5 more
TL;DR: It is proposed that one function of TGF-beta 1 during endochondral ossification is regulation of chondrocyte growth and differentiation through modulation of the relative expression of cartilage matrix proteins and metalloproteases.
Transforming growth factors from neoplastic and nonneoplastic tissues.
TL;DR: TGF-beta, isolated from bovine sources, accelerates experimental wound healing in rats and can be classified as type alpha or type beta based on their interactions with the receptor for epidermal growth factor and their requirement for EGF (or an EGF-like polypeptide) for functional activity.