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Kathleen C. Flanders

Researcher at National Institutes of Health

Publications -  150
Citations -  19846

Kathleen C. Flanders 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 68, co-authored 150 publications receiving 19278 citations. Previous affiliations of Kathleen C. Flanders include Gyeongsang National University & New York State Department of Health.

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Transforming growth factor beta 1 null mutation in mice causes excessive inflammatory response and early death.

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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Evidence that transforming growth factor-β is a hormonally regulated negative growth factor in human breast cancer cells

TL;DR: In MCF-7 cells, TGF-beta is a hormonally regulated growth inhibitor with possible autocrine and paracrine functions in breast cancer cells, and growth inhibition is reversed with anti-TGF- beta antibodies.
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Role of transforming growth factor-beta in the development of the mouse embryo.

TL;DR: Using immunohistochemical methods, the role of transforming growth factor-beta (TGF-beta) in the development of the mouse embryo is investigated and its ability to control both synthesis and degradation of both structural and adhesion molecules of the extracellular matrix is discussed.
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Latent transforming growth factor-beta from human platelets. A high molecular weight complex containing precursor sequences.

TL;DR: The latent TGF-beta secreted by platelets may be a cellular delivery complex, whereas the latent form found in serum may represent a clearance complex, and alpha 2M may scavenge excess T GF-beta that is released when the platelet latent form is activated, possibly by the clotting process.
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Transforming growth factor beta 1 positively regulates its own expression in normal and transformed cells.

TL;DR: It is reported that TGF-beta 1 increases steady-state levels of its own message in six different normal and transformed cells in culture.