Blocking Smad7 restores TGF-beta1 signaling in chronic inflammatory bowel disease.
By G. Monteleone, A. Kumberová, N. Croft, C. McKenzie, H. Steer, T. Macdonald. Journal of Clinical Investigation, 2001
612 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/e167146c2170b109d963fe6a577c33fbfe3489e8
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Citations in the corpus
- Innate and adaptive immunity in inflammatory bowel disease. (2014, background): “An intact TGF-β signaling, which is impaired in inflamed IBDmucosa because of the up-regulation of the inhibitorymolecule Smad7, is required for Treg function [88,89].”
- TGF-beta and fibrosis in different organs - molecular pathway imprints. (2009, background): “rylated (phospho-) Smad3 was observed which was rapidly upregulated by the addition of exogenous TGF-β1 [91].”
- Cytokine Networks in the Pathophysiology of Inflammatory Bowel Disease. (2019, background): “Early studies showed that T cells from the inflamed IBD mucosa express high amounts of Smad7 and are unresponsive to TGF-β1.”
- Mechanisms of Disease: pathogenesis of Crohn's disease and ulcerative colitis (2006, background): “A potential mechanism of acquired defects in regulatory function has been suggested by MacDonald, who reported induction of SMAD7 expression in patients with active disease”
- TGF-β Activation and Function in Immunity (2013, background): “cytokine expression in these cells (32), at least in part by enabling suppression by regulatory”
- The immunological and genetic basis of inflammatory bowel disease (2003, background): “cgi?l=4092">SMAD7 — a known repressor of TGF-β signallin”
- Smad3 as a mediator of the fibrotic response (2004, background): “Monteleone et al. (2001) have reported that in active lesions from patients with inflammatory bowel disease, there was increased expression of Smad7 protein that was not present in areas of endoscopically normal mucosa from the same patients.”