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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.

Papers
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Journal Article

Induction of hyperplasia and its suppression by hydrocortisone in organ-cultured rat urinary bladder.

TL;DR: Urinary bladders from Fischer rats organ cultured in a chemically defined medium, Ham's F12, underwent transitional cell hyperplasia which persisted for the duration of the culture period (10 days), and the hyperplastic response in the transitional epithelium was significantly inhibited by hydrocortisone.
Journal ArticleDOI

Distinct Regulations of HO-1 Gene Expression for Stress Response and Substrate Induction

TL;DR: In this paper, the HO-1-DsRed-knock-in reporter mouse was used to study the role of the DsRed gene in the HO1-DsRed fusion protein in peritoneal macrophages.
Book ChapterDOI

Interactions of Retinoids and Transforming Growth Factor-Beta in the Chemoprevention of Cancer

TL;DR: The conventional clinical approach with most epithelial cancer has been to wait until the patient has invasive disease and then treat this disease with cytotoxic chemotherapy, surgery, or radiation; none of these modalities has been uniquely successful for the treatment of all types of epithelialcancer.
Patent

Synthetic triterpenoids and methods for modulating stem/progenitor cell gene expression

TL;DR: Synthetic triterpenoids and methods of using the same to induce gene expression and differentiation of stem or progenitor cells are provided in this paper, where a method for producing a cell such as a stem or pro-germanic cell with induced gene expression by contacting a stem/progenitor cell with an effective amount of a synthetic triterpoid to induce the expression of one or more of SOX9 (Sex determining region Y-box 9), COL2A1 (Type II Collagen (alpha1)), TGF-βI, TGF