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Author

Michael B. Sporn

Bio: 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 ArticleDOI
TL;DR: In this article, title compound (I) is easily synthesized as first example of an oleane triterpenoid anhydride and it is shown that it can be used to synthesize triterpene anhydrides.
Abstract: Title compound (I) is easily synthesized as first example of an oleane triterpenoid anhydride.
Book ChapterDOI
01 Jan 1983
TL;DR: In this paper, the authors used a μBondapak C 18 column with an acetonitrile gradient to resolve TGF activity into two peaks, one of which requires epidermal growth factor (EGF) to induce colony formation of indicator cells in soft agar.
Abstract: Transforming growth factors (TGF) are low molecular weight, acid-stable polypeptides that confer a malignant phenotype on nonneoplastic cells. TGF from murine sarcoma virus transformed 3T3 cells were isolated by acid/ethanol extraction, Bio-Gel P-30 chromatography, and reverse-phase high-performance liquid chromatography. Using a μBondapak C 18 column with an acetonitrile gradient, TGF activity can be resolved into two peaks, one of which requires epidermal growth factor (EGF) to induce colony formation of indicator cells in soft agar. Subsequent rechromatography of the EGF-dependent TGF on a μBondapak CN column using an n-propanol gradient resulted in a 430-fold purification over the acid/ethanol extract and showed soft agar activity at a concentration of 4 ng/ml in the presence of 2 ng/ml EGF. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed one main band with an apparent molecular weight of 13,000.
Patent
18 Jun 1999
TL;DR: In this article, the present invention relates to a compound having formula: "premature" where either A or B is a double-bond such that when A was a double bond, C 11 has substituted thereon =X, and when B was an inorganic moiety selected from amino, thiol, and hydroxyl (tantamount to =X being =NH, =S, or =O).
Abstract: The present invention relates to a compound having formula: wherein (a) either A or B is a double bond such that when A is a double bond, C 11 has substituted thereon =X, and when B is a double bond, C 12 has substituted thereon =X, X being an inorganic moiety selected from amino, thiol, and hydroxyl (tantamount to =X being =NH, =S, or =O); (b) R 1 is an electron-withdrawing moiety selected from cyano, -COOH, and halogen; (c) R x is methyl; and (d) Y is hydrogen, an inorganic moiety selected from halogen, amino, and hydroxyl, or an organic moiety selected from alkyl, alkylamino, alkoxy, and aryl.

Cited by
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Journal ArticleDOI
07 Jan 2000-Cell
TL;DR: This work has been supported by the Department of the Army and the National Institutes of Health, and the author acknowledges the support and encouragement of the National Cancer Institute.

28,811 citations

28 Jul 2005
TL;DR: PfPMP1)与感染红细胞、树突状组胞以及胎盘的单个或多个受体作用,在黏附及免疫逃避中起关键的作�ly.
Abstract: 抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1(PfPMP1)与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用,在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员,通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

18,940 citations

Journal ArticleDOI
29 Apr 1993-Nature
TL;DR: The ability to control the expression of genes encoding these molecules and to target specific cell types provides opportunities to develop new diagnostic and therapeutic agents to induce the regression of the lesions and, possibly, to prevent their formation.
Abstract: Atherosclerosis, the principal cause of heart attack, stroke and gangrene of the extremities, is responsible for 50% of all mortality in the USA, Europe and Japan. The lesions result from an excessive, inflammatory-fibroproliferative response to various forms of insult to the endothelium and smooth muscle of the artery wall. A large number of growth factors, cytokines and vasoregulatory molecules participate in this process. Our ability to control the expression of genes encoding these molecules and to target specific cell types provides opportunities to develop new diagnostic and therapeutic agents to induce the regression of the lesions and, possibly, to prevent their formation.

10,861 citations

Journal ArticleDOI
19 Mar 2010-Cell
TL;DR: The principal mechanisms that govern the effects of inflammation and immunity on tumor development are outlined and attractive new targets for cancer therapy and prevention are discussed.

8,664 citations

Journal ArticleDOI
TL;DR: The transforming growth factor beta (TGF-beta) family of growth factors control the development and homeostasis of most tissues in metazoan organisms and mutations in these pathways are the cause of various forms of human cancer and developmental disorders.
Abstract: The transforming growth factor beta (TGF-beta) family of growth factors control the development and homeostasis of most tissues in metazoan organisms. Work over the past few years has led to the elucidation of a TGF-beta signal transduction network. This network involves receptor serine/threonine kinases at the cell surface and their substrates, the SMAD proteins, which move into the nucleus, where they activate target gene transcription in association with DNA-binding partners. Distinct repertoires of receptors, SMAD proteins, and DNA-binding partners seemingly underlie, in a cell-specific manner, the multifunctional nature of TGF-beta and related factors. Mutations in these pathways are the cause of various forms of human cancer and developmental disorders.

7,710 citations