Smurf
Mostrando 1-12 de 12 artigos, teses e dissertações.
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1. TGFbeta, activina e sinalização SMAD em câncer de tiróide
TGFbeta e activina são membros da superfamília TGFbeta e desempenham um amplo papel no desenvolvimento, proliferação e apoptose. Estes fatores de crescimento exercem seus efeitos biológicos ligando-se a receptores de membrana do tipo I e do tipo II que transduzem a sinalização até o núcleo através da fosforilação das proteínas R-SMADs (SMAD 2/3)
Arquivos Brasileiros de Endocrinologia & Metabologia. Publicado em: 2007-07
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2. Cooperative Inhibition of Bone Morphogenetic Protein Signaling by Smurf1 and Inhibitory Smads
Smad ubiquitin regulatory factor (Smurf) 1 binds to receptor-regulated Smads for bone morphogenetic proteins (BMPs) Smad1/5 and promotes their degradation. In addition, Smurf1 associates with transforming growth factor-β type I receptor through the inhibitory Smad (I-Smad) Smad7 and induces their degradation. Herein, we examined whether Smurf1 negativel
The American Society for Cell Biology.
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3. Cerebral Cavernous Malformation 2 Protein Promotes Smad Ubiquitin Regulatory Factor 1-mediated RhoA Degradation in Endothelial CellsS⃞
Mutation of CCM2 predisposes individuals to cerebral cavernous malformations, vascular abnormalities that cause seizures and hemorrhagic stroke. CCM2 has been proposed to regulate the activity of RhoA for maintenance of vascular integrity. Herein, we define a novel mechanism where the CCM2 phosphotyrosine binding (PTB) domain binds the ubiquitin ligase (
American Society for Biochemistry and Molecular Biology.
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4. Smurf2 up-regulation activates telomere-dependent senescence
Progressive telomere shortening activates replicative senescence, which prevents somatic cells from being propagated indefinitely in culture. The limitation of proliferative capacity imposed by replicative senescence is thought to contribute to both organismal aging and the prevention of tumor development. Here we report that up-regulation of Smurf2, an E3 u
Cold Spring Harbor Laboratory Press.
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5. Smurf2 Participates in Human Trophoblast Cell Invasion by Inhibiting TGF-β Type I Receptor
Successful embryo implantation depends on the ability of the trophoblast cells to invade the endometrium and the receptivity of the endometrium. Unlike tumor invasion, trophoblast invasion is spatio-temporaly restricted. Transforming growth factor (TGF)-β is a key inhibitory factor in the invasion of early trophoblast cells. Smad ubiquitination regulatory f
Histochemical Society.
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6. Regulation of Smad degradation and activity by Smurf2, an E3 ubiquitin ligase
Smad proteins are key intracellular signaling effectors for the transforming growth factor-β superfamily of peptide growth factors. Following receptor-induced activation, Smads move into the nucleus to activate transcription of a select set of target genes. The activity of Smad proteins must be tightly regulated to exert the biological effects of diffe
The National Academy of Sciences.
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7. Impaired Smad7-Smurf–mediated negative regulation of TGF-β signaling in scleroderma fibroblasts
The principal effect of TGF-β1 on mesenchymal cells is its stimulation of ECM synthesis. Previous reports indicated the significance of the autocrine TGF-β loop in the pathogenesis of scleroderma. In this study, we focused on Smad7 and Smurfs, principal molecules in the negative regulation of TGF-β signaling, to further understand the autocrine TGF-β loo
American Society for Clinical Investigation.
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8. Role of SARA (SMAD Anchor for Receptor Activation) in Maintenance of Epithelial Cell Phenotype*
By inducing epithelial-to-mesenchymal transition (EMT), transforming growth factor-β (TGF-β) promotes cancer progression and fibrosis. Here we show that expression of the TGF-β receptor-associated protein, SARA (Smad anchor for receptor activation), decreases within 72 h of exposure to TGF-β and that this decline is both required and sufficient for the i
American Society for Biochemistry and Molecular Biology.
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9. Smad6 Inhibits the Transcriptional Activity of Tbx6 by Mediating Its Degradation*
Members of the bone morphogenetic protein (BMP) and T-box gene families play several critical roles in the early embryonic development and tissue homeostasis. Although BMP proteins are the upstream regulators of T-box genes, few studies have investigated the molecular mechanisms between these two protein families. Here, we report that Tbx6 interacts directly
American Society for Biochemistry and Molecular Biology.
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10. Down-regulation of Smad7 expression by ubiquitin-dependent degradation contributes to renal fibrosis in obstructive nephropathy in mice
Overexpression of transforming growth factor β (TGF-β) has been shown to play pathogenic roles in progression of renal fibrosis, and the severity of tubulointerstitial fibrosis correlates better with renal function than the severity of glomerulosclerosis. Smad proteins are signaling transducers downstream from TGF-β receptors. Three families of Smad prote
National Academy of Sciences.
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11. Arkadia amplifies TGF-β superfamily signalling through degradation of Smad7
Arkadia was originally identified as a protein that enhances signalling activity of Nodal and induces mammalian nodes during early embryogenesis; however, the mechanisms by which Arkadia affects transforming growth factor-β (TGF-β) superfamily signalling have not been determined. Here we show that Arkadia is widely expressed in mammalian tissues, and that
Oxford University Press.
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12. Hepatocyte Growth Factor Inhibits Epithelial to Myofibroblast Transition in Lung Cells via Smad7
Idiopathic pulmonary fibrosis is a lethal parenchymal lung disease characterized by denudation of the lung epithelium, fibroblast proliferation, and collagen deposition. Cellular changes underlying disease progression involve injury to alveolar epithelial cells, epithelial to mesenchymal transition, proliferation of α-smooth muscle actin (α-SMA)–expressi
American Thoracic Society.