Results 41 to 50 of about 55,562 (295)

Mutations in protein-binding hot-spots on the hub protein Smad3 differentially affect its protein interactions and Smad3-regulated gene expression. [PDF]

open access: yesPLoS ONE, 2011
Hub proteins are connected through binding interactions to many other proteins. Smad3, a mediator of signal transduction induced by transforming growth factor beta (TGF-β), serves as a hub protein for over 50 protein-protein interactions.
Michelle M Schiro   +8 more
doaj   +1 more source

FoxO3 normalizes Smad3-induced arterial smooth muscle cell growth

open access: yesFrontiers in Physiology, 2023
Transition of arterial smooth muscle (ASM) from a quiescent, contractile state to a growth-promoting state is a hallmark of cardiovascular disease (CVD), a leading cause of death and disability in the United States and worldwide.
Jake T. Francisco   +7 more
doaj   +1 more source

SMAD3 promotes autophagy dysregulation by triggering lysosome depletion in tubular epithelial cells in diabetic nephropathy

open access: yesAutophagy, 2020
Macroautophagy/autophagy dysregulation has been noted in diabetic nephropathy; however, the regulatory mechanisms controlling this process remain unclear.
Chen Yang   +9 more
semanticscholar   +1 more source

Cathepsin L-mediated resistance of paclitaxel and cisplatin is mediated by distinct regulatory mechanisms

open access: yesJournal of Experimental & Clinical Cancer Research, 2019
Background Cathepsin L (CTSL) is a cysteine protease known to have important roles in regulating cancer cellular resistance to chemotherapy. However mechanism underlying which regulates CTSL-mediated drug resistance remain largely unknown.
Yifan Zhao   +10 more
doaj   +1 more source

Smad3 promotes AKI sensitivity in diabetic mice via interaction with p53 and induction of NOX4-dependent ROS production

open access: yesRedox Biology, 2020
The incidence and severity of acute kidney injury (AKI) is increased yearly in diabetic patients. Although the mechanisms for this remain unclear, the prevention of AKI in diabetic nephropathy is feasible and of value. As we detected highly activation of
Jia-nan Wang   +18 more
semanticscholar   +1 more source

Fibrotic scar formation after cerebral ischemic stroke: Targeting the Sonic hedgehog signaling pathway for scar reduction

open access: yesNeural Regeneration Research
Recent studies have shown that fibrotic scar formation following cerebral ischemic injury has varying effects depending on the microenvironment. However, little is known about how fibrosis is induced and regulated after cerebral ischemic injury.
Jun Wen   +16 more
doaj   +1 more source

Smad3 Regulates Neuropilin 2 Transcription by Binding to its 5′ Untranslated Region

open access: yesJournal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 2020
Background Vascular smooth muscle cell phenotypic change and consequential intimal hyperplasia (IH) cause arterial stenosis and posttreatment restenosis.
Xiujie Xie   +5 more
doaj   +1 more source

Redirecting RNA splicing by SMAD3 turns TGF-β into a tumor promoter

open access: yesMolecular & Cellular Oncology, 2017
Transforming growth factor β (TGF-β) is a well-known growth inhibitor of normal epithelial cells, but it is also secreted by solid tumors to promote cancer progression.
Veenu Tripathi, Ying E. Zhang
doaj   +1 more source

Endothelial dysfunction exacerbates renal interstitial fibrosis through enhancing fibroblast Smad3 linker phosphorylation in the mouse obstructed kidney. [PDF]

open access: yesPLoS ONE, 2013
Endothelial dysfunction and enhanced transforming growth factor-β (TGF-β)/Smad3 signalling are common features of progressive renal fibrosis. This study investigated a potential link between these mechanisms.
Yu Bo Yang Sun   +4 more
doaj   +1 more source

SMAD3 mutation in LDS3 causes bone fragility by impairing the TGF-β pathway and enhancing osteoclastogenesis

open access: yesBone Reports, 2022
Loss-of-function mutations in SMAD3 cause Loeys-Dietz syndrome type 3 (LDS3), a rare autosomal-dominant connective tissue disorder characterized by vascular pathology and skeletal abnormalities.
Ahmed El-Gazzar   +12 more
doaj   +1 more source

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