Role of transforming growth factor beta in human disease.

By G. Blobe, W. Schiemann, H. Lodish. New England Journal of Medicine, 2000

2,472 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/58a1c5bb2518808022280d50de2d011804fd7883

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Citations in the corpus

TGF-beta and fibrosis in different organs - molecular pathway imprints. (2009, background): “in intestinal homeostasis as a negative master regulator of inflammation is well-established [77,78] and indisputable.”
SB-431542 is a potent and specific inhibitor of transforming growth factor-beta superfamily type I activin receptor-like kinase (ALK) receptors ALK4, ALK5, and ALK7. (2002, background): “Aberrant signaling by TGF- , the prototype of the family, has been implicated in a number of human diseases, including cancer, hereditary hemorrhagic telangiectasia, atherosclerosis, and fibrotic disease of the kidney, liver, and lung (Blobe et al., 2000).”
Making sense of latent TGFβ activation (2003, background): “Defects in TGFβ function are associated with a number of pathological states, including tumor cell growth, fibrosis and autoimmune disease (Blobe et al., 2000).”
TGF-beta: a master of all T cell trades. (2008, neutral): “as embryogenesis, carcinogenesis, and the immune response (Blobe et al., 2000).”
The biphasic function of microglia in ischemic stroke (2017, neutral): “Studies showed that TGF-b could induce microglia polarization to M2 phenotype (Blobe et al., 2000; Hanisch and Kettenmann, 2007).”
Fibronectin is required for integrin o:vβ6‐mediated activation of latent TGF‐β complexes containing LTBP‐1 (2005, background): “Anomalous regulation of TGF- activity has been related to several human diseases, including tumorigenesis, fibrosis, and autoimmune disease (6).”