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postnatal ablation of Smad4 caused various vascular defects, including the formation of distinct arteriovenous malformations in the neonate retina.
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These findings indicate that PDZK1IP1 interacts with Smad4 and thereby suppresses the TGF-beta signaling pathway.
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Cell-permeable SBD peptide blocked the association of p65 with Smad4 and enhanced BMP2-induced osteoblast differentiation and mineralization.
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Postnatal endothelial Smad4 ablation causes AVM formation in retinas. SMAD4 attenuates CK2 expression and counteracts flow-induced PI3K/AKT1 signaling to prevent arteriovenous malformations formation.
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These results indicate that SMAD4 functions to maintain differentiated enterocytes in the presence of oncogenic WNT signaling, thus preventing dedifferentiation and tumor formation in the differentiated intestinal epithelium
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study identifies and mechanistically characterizes unusual functions and pathways for SMAD4 in governing innate immune responses to cancer and viral infection, as well as NK cell development.
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This stimulation by BMP7 was lost in the combined TGFBR2 and SMAD4 double knockout fibroblasts, which included a profound decrease in HGF expression. Thus, Smad4-mediated signaling is required to initiate epithelial carcinogenesis subsequent to TGFBR2 deletion in FSP1(+) fibroblasts.
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TGFbeta suppresses the expression of proinflammatory genes in the colon epithelium, and loss of its downstream mediator, SMAD4, is sufficient to initiate inflammation-driven colon cancer.
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HNF4A acts redundantly with an intestine-restricted HNF4 paralog, HNF4G, to activate enhancer chromatin and upregulate the majority of transcripts in the differentiated epithelium; cells fail to differentiate on double knockout of both HNF4 paralogs. Furthermore, we show that SMAD4 and HNF4 function via a reinforcing feed-forward loop.
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This review lists SMAD4 mutations in various types of cancer and summarizes recent advances on SMAD4 with focuses on the function, signaling pathway, and the possibility of SMAD4 as a prognostic indicator. [review]
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To uncover the molecular changes induced by the concurrent targeting of E-cadherin, p53, and Smad4 loss.
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These results suggest a new mechanism whereby Smad4 controls chondrocyte hypertrophy by up-regulating Runx2 expression during skeletal development. The regulatory mechanism involving Smad4-mediated Runx2 activation uncovered here provides critical insights into bone development and pathogenesis of chondrodysplasia.
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The significant insight into synergistic role of Pten and Smad4 in SGT.
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Smad4 deletion may inhibit lipogenesis, stimulate beta-oxidation, improve lipid metabolism and liver function, alleviate inflammation and fibrosis, and reduce cell apoptosis in nonalcoholic steatohepatitis
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Loss of Smad4 in neural progenitor cells impairs adult neurogenesis in the subventricular zone.
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Reduced bone-mass and accelerated osteoclastogenesis seen in Smad4-cKO were abrogated by Prdm1 deletion. Administration of latent-TGFbeta1-Fc to wild-type mice antagonized LPS-induced bone destruction in a model of activated osteoclast-mediated bone destruction
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miR146b5p directly targeted Smad4 and negatively regulated the transforming growth factor (TGF)-beta signaling pathway, which contributed to the neural commitment of Pluripotent stem cells (PSCs). Collectively, our findings uncover the essential role of miR146b5p in the neural conversion of PSCs.
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study reveals a critical mechanism by which TGFbeta controls TH17 cell differentiation and uncovers the SKI-SMAD4 axis as a potential therapeutic target for treating TH17-related diseases
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The binding motif of miR26b5p in the Smad4 3'UTR was identified as UACUUGA at position 978-984.
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Smad4 expression in T lymphocytes plays a protective role in the development of autoimmune Sjogren's syndrome in the nonobese diabetic mouse.