R
Ronald A. Ignotz
Researcher at University of Massachusetts Medical School
Publications - 32
Citations - 6277
Ronald A. Ignotz is an academic researcher from University of Massachusetts Medical School. The author has contributed to research in topics: Transforming growth factor & Transforming growth factor beta. The author has an hindex of 23, co-authored 32 publications receiving 6119 citations. Previous affiliations of Ronald A. Ignotz include University of Massachusetts Amherst.
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Transforming growth factor-beta stimulates the expression of fibronectin and collagen and their incorporation into the extracellular matrix.
Ronald A. Ignotz,Joan Massagué +1 more
TL;DR: The results demonstrate a functional involvement of fibronectin in mediating cellular responses to TGFbeta, and suggest a model for TGF beta action based on the control of the extracellular matrix in target cells.
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Regulation of fibronectin and type I collagen mRNA levels by transforming growth factor-beta.
TL;DR: The results indicate that TGF-beta 1 controls the composition and abundance of extracellular matrices at least in part by inducing a coordinate increase in the levels of fibronectin and type I collagen mRNAs.
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Regulation of cell adhesion receptors by transforming growth factor-beta. Concomitant regulation of integrins that share a common beta 1 subunit.
TL;DR: In this article, the authors examined the effect of transforming growth factor-beta 1 on the expression of the very late antigens or alpha beta 1 group of integrins in human cell lines.
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Cell adhesion protein receptors as targets for transforming growth factor-β action
Ronald A. Ignotz,Joan Massagué +1 more
TL;DR: The results show that the expression of cell adhesion receptors is susceptible to pretranslational and posttranslational regulation by factors that control cell morphology, proliferation, and differentiation such as TGF-beta.
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Type beta transforming growth factor controls the adipogenic differentiation of 3T3 fibroblasts
Ronald A. Ignotz,Joan Massagué +1 more
TL;DR: It is found that TGF-beta inhibits potently (ID50 approximately equal to 25 pM) the adipogenic conversion of 3T3-L1 cells, suggesting that T GF-beta is a unique modulator of adipogenic differentiation of fibroblasts.