Results 261 to 270 of about 55,562 (295)
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Smad3 phosphorylation by cyclin-dependent kinases
Cytokine & Growth Factor Reviews, 2006Smad3, a key mediator for TGF-beta antiproliferative responses, is phosphorylated by both CDK4 and CDK2 in vivo and in vitro. Except for the Rb family members, Smad3 is the only CDK4 substrate demonstrated so far. CDK phosphorylation of Smad3 inhibits its transcriptional activity and antiproliferative function.
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Biochemical and Biophysical Research Communications, 2001
Regulation of subcellular localization of Smad proteins is supposed to be critical for the effective initiation and maintenance of TGF-beta signaling. Recently, Smad anchor for receptor activation (SARA) has been identified as a Smad2 binding protein.
D. Goto +5 more
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Regulation of subcellular localization of Smad proteins is supposed to be critical for the effective initiation and maintenance of TGF-beta signaling. Recently, Smad anchor for receptor activation (SARA) has been identified as a Smad2 binding protein.
D. Goto +5 more
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Journal of Medical Genetics, 2019
Background Pathogenic variants in SMAD3 cause thoracic aortic aneurysms and dissections, along with aneurysms and rupture of other arteries. Here, we examined differences in clinical presentation of aortic events (dissection or surgical repair of an ...
Ellen M. Hostetler +16 more
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Background Pathogenic variants in SMAD3 cause thoracic aortic aneurysms and dissections, along with aneurysms and rupture of other arteries. Here, we examined differences in clinical presentation of aortic events (dissection or surgical repair of an ...
Ellen M. Hostetler +16 more
semanticscholar +1 more source
Science Translational Medicine, 2018
A human long noncoding RNA targeting the TGF-β/Smad pathway reduced fibrogenesis in mouse models of renal fibrosis. A target for renal fibrosis Transforming growth factor–β (TGF-β) is a known regulator of fibrosis but has remained difficult to target ...
Peng Wang +10 more
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A human long noncoding RNA targeting the TGF-β/Smad pathway reduced fibrogenesis in mouse models of renal fibrosis. A target for renal fibrosis Transforming growth factor–β (TGF-β) is a known regulator of fibrosis but has remained difficult to target ...
Peng Wang +10 more
semanticscholar +1 more source
Regulation of Renal Fibrosis by Smad3 Thr388 Phosphorylation
The American Journal of Pathology, 2014Transforming growth factor-β (TGF-β) promotes tissue fibrosis via receptor-mediated phosphorylation of the receptor-activated Smad2/3, together with Smad4. Of these, Smad3 plays a major profibrotic role in mouse models of tissue fibrosis. Transcriptional activity of the Smad3 protein is regulated by phosphorylation of residues in the C-terminal domain ...
Xinli, Qu +7 more
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Aberrant expression of p-Smad3 in oral carcinogenesis
Clinical Oral Investigations, 2014Smads are the keys of transforming growth factor β (TGFβ) signaling cascade and play a crucial role in many cancers. Once TGFβ receptors are activated, Smad2 and Smad3 are phosphorylated and form complexes with Smad4. These complexes translocate from the cytoplasm to the nucleus where they regulate the target genes.
Sopee, Poomsawat +2 more
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New insights into Smad3 in cardiac fibrosis
GeneDamage to myocardial tissues, leading to myocardial fibrosis, is a significant pathological hallmark across various heart diseases. SMAD3, a central transcriptional regulator within the transforming growth factor-beta (TGF-β) signaling pathway, plays a pivotal role in the pathological progression of myocardial fibrosis and cardiac remodeling.
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