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Anita B. Roberts
Researcher at National Institutes of Health
Publications - 342
Citations - 77632
Anita B. Roberts is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Transforming growth factor & Transforming growth factor beta. The author has an hindex of 138, co-authored 342 publications receiving 76037 citations. Previous affiliations of Anita B. Roberts include MSC Industrial Direct Company, Inc..
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Journal ArticleDOI
Transforming growth factor type beta: rapid induction of fibrosis and angiogenesis in vivo and stimulation of collagen formation in vitro.
Anita B. Roberts,Michael B. Sporn,Richard K. Assoian,J M Smith,Nanette S. Roche,Lalage M. Wakefield,U. Heine,Lance A. Liotta,Vincent Falanga,John H. Kehrl +9 more
TL;DR: Further data are obtained to support a role for TGF-beta as an intrinsic mediator of collagen formation: conditioned media obtained from activated human tonsillar T lymphocytes contain greatly elevated levels of T GF-beta compared tomedia obtained from unactivated lymphocytes.
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Transforming growth factor beta 1 null mutation in mice causes excessive inflammatory response and early death.
Ashok B. Kulkarni,Chang-Goo Huh,Dean Becker,Andrew G. Geiser,Marion Lyght,Kathleen C. Flanders,Anita B. Roberts,Michael B. Sporn,Jerrold M. Ward,Stefan Karlsson +9 more
TL;DR: Pathological examination revealed an excessive inflammatory response with massive infiltration of lymphocytes and macrophages in many organs, but primarily in heart and lungs, which suggests a prominent role for TGF-beta 1 in homeostatic regulation of immune cell proliferation and extravasation into tissues.
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Endothelial-to-mesenchymal transition contributes to cardiac fibrosis
Elisabeth M. Zeisberg,Oleg Tarnavski,Michael Zeisberg,Adam L. Dorfman,Julie R. McMullen,Erika Gustafsson,Anil Chandraker,Xueli Yuan,William T. Pu,Anita B. Roberts,Eric G. Neilson,Mohamed H. Sayegh,Seigo Izumo,Raghu Kalluri +13 more
TL;DR: It is shown that cardiac fibrosis is associated with the emergence of fibroblasts originating from endothelial cells, suggesting an endothelial-mesenchymal transition (EndMT) similar to events that occur during formation of the atrioventricular cushion in the embryonic heart.
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REGULATION OF IMMUNE RESPONSES BY TGF-β*
TL;DR: The accumulated knowledge gained through extensive in vitro functional analyses and from in vivo animal models supports the concept that clinical therapies based on modulation of this cytokine represent an important new approach to the treatment of disorders of immune function.