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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

SKI-like oncogene

SnoN, S-NO
The protein encoded by this gene is a component of the SMAD pathway, which regulates cell growth and differentiation through transforming growth factor-beta (TGFB). In the absence of ligand, the encoded protein binds to the promoter region of TGFB-responsive genes and recruits a nuclear repressor complex. TGFB signaling causes SMAD3 to enter the nucleus and degrade this protein, allowing these genes to be activated. Four transcript variants encoding three different isoforms have been found for this gene. [provided by RefSeq, Oct 2011] (from NCBI)
Top mentioned proteins: Cdc7, TGF-beta, CAN, Smad2, V1a
Papers on SnoN
Inducible NO synthase is constitutively expressed in porcine myocardium and its level decreases along with tachycardia-induced heart failure.
Michlik et al., Wrocław, Poland. In Cardiovasc Pathol, Jan 2016
Thus, it can be assumed that an up-regulation of proinflammatory factors is not involved in porcine tachycardia-induced cardiomyopathy and that the impact of oxidative stress may be restricted to the mitochondria in this HF model.
The downregulation of SnoN expression in human renal proximal tubule epithelial cells under high-glucose conditions is mediated by an increase in Smurf2 expression through TGF-β1 signaling.
Liu et al., Beijing, China. In Int J Mol Med, Jan 2016
Previous studies have demonstrated that the Smad transcriptional co-repressor, Ski-related novel protein N (SnoN), an antagonizer of TGF-β1/Smad signaling, is downregulated in the kidneys of diabetic rats; however, the underlying molecular mechanisms remain elusive.
An efficient S-NO-polysilsesquioxane nano-platform for the co-delivery of nitric oxide and an anticancer drug.
Hu et al., Taipei, Taiwan. In Chem Commun (camb), Dec 2015
Here, we report a one-step nanoprecipitation method to generate nanoparticles that possess simultaneous NO-donating and doxorubicin releasing properties.
S-Nitrosylation of Sarcomeric Proteins Depresses Myofilament Ca(2+) Sensitivity in Intact Cardiomyocytes.
Pinto et al., Rio de Janeiro, Brazil. In Antioxid Redox Signal, Dec 2015
In live cardiomyocytes treated with CysNO, resin-assisted capture of S-nitrosylated protein thiols was combined with label-free liquid chromatography-tandem mass spectrometry to quantify S-nitrosylation and determine the susceptible cysteine sites on myosin, actin, myosin-binding protein C, troponin C and I, tropomyosin, and titin.
Maid is a negative regulator of transforming growth factor-β-induced cell migration.
Miyazawa et al., Japan. In J Biochem, Nov 2015
Notably, Maid expression was induced in the delayed phase (later than 24 h) after TGF-β stimulation whereas the expression of two other negative feedback regulators, Smad7 and SnoN, was induced as early as 1 h after stimulation.
Genistein suppressed epithelial-mesenchymal transition and migration efficacies of BG-1 ovarian cancer cells activated by estrogenic chemicals via estrogen receptor pathway and downregulation of TGF-β signaling pathway.
Hwang et al., Ch'ŏngju, South Korea. In Phytomedicine, Nov 2015
In the protein expression of SnoN and Smad3, E2, BPA, and NP upregulated SnoN, a negative regulator of TGF-β signaling, and downregulated pSmad3, a transcription factor in the downstream pathway of TGF-β signaling pathway, suggesting that E2, BPA, and NP simultaneously lead to the downregualtion of TGF-β signaling in the process of induction of EMT and migration of BG-1 cells via ER signaling.
Transforming growth factor-β signaling pathway cross-talking with ERα signaling pathway on regulating the growth of uterine leiomyoma activated by phenolic environmental estrogens in vitro.
Ren et al., Nanjing, China. In Tumour Biol, Aug 2015
Subsequently, qRT-PCR was applied to detect mRNA expressions of ERα and c-fos, while western blot assay was used to test the expressions of p-Smad3, SnoN, and c-fos proteins in all settings mentioned above; the expressions were compared among different groups, and also in settings with and without synchronous treatment of ICI 182,780.
SnoN as a novel negative regulator of TGF-β/Smad signaling: a target for tailoring organ fibrosis.
Dixon et al., Winnipeg, Canada. In Am J Physiol Heart Circ Physiol, Feb 2015
SnoN (and its alternatively-spliced isoforms SnoN2, SnoA, and SnoI) is one of four members of a family of negative regulators of TGF-β1 signaling that includes Ski and functional Smad-suppressing elements on chromosomes 15 and 18. SnoN has been shown to be structurally and functionally similar to Ski and has been demonstrated to directly interact with Ski to abrogate gene expression.
Methods for detection and characterization of protein S-nitrosylation.
Chen et al., Taipei, Taiwan. In Methods, 2013
Reversible protein S-nitrosylation, defined as the covalent addition of a nitroso moiety to the reactive thiol group on a cysteine residue, has received increasing recognition as a critical post-translational modification that exerts ubiquitous influence in a wide range of cellular pathways and physiological processes.
Protein s-nitrosylation measurement.
Daaka et al., Gainesville, United States. In Methods Enzymol, 2012
In this review, we summarize current methods for detection of protein S-nitrosylation with a focus on the biotin switch technique and related methods.
S-nitrosation/denitrosation in cardiovascular pathologies: facts and concepts for the rational design of S-nitrosothiols.
Leroy et al., Nancy, France. In Curr Pharm Des, 2012
Disulfide forming/ isomerizing enzymes like thioredoxin (Trx), protein disulfide isomerase (PDI), which are chaperone proteins, are implicated into transnitrosation reactions, which are the transfer of •NO from one cysteine residue to another one.
SnoN regulates mammary gland alveologenesis and onset of lactation by promoting prolactin/Stat5 signaling.
Luo et al., Berkeley, United States. In Development, 2012
SnoN, a negative regulator of TGF-beta signaling, coordinates TGF-beta and prolactin signaling to control alveologenesis and lactogenesis.
SnoN suppresses maturation of chondrocytes by mediating signal cross-talk between transforming growth factor-β and bone morphogenetic protein pathways.
Komiya et al., Kagoshima, Japan. In J Biol Chem, 2012
SnoN mediates a negative feedback mechanism evoked by TGF-beta to inhibit BMP signaling and, subsequently, hypertrophic maturation of chondrocytes.
Transforming growth factor-β/SMAD Target gene SKIL is negatively regulated by the transcriptional cofactor complex SNON-SMAD4.
Macías-Silva et al., Mexico. In J Biol Chem, 2012
the SNON-SMAD4 complex negatively regulated basal SKIL gene expression through binding the promoter and recruiting histone deacetylases
SnoN in regulation of embryonic development and tissue morphogenesis.
Luo et al., Berkeley, United States. In Febs Lett, 2012
SnoN may have broad functions in the embryonic development and tissue morphogenesis [Review]
SnoN signaling in proliferating cells and postmitotic neurons.
Bonni et al., Calgary, Canada. In Febs Lett, 2012
analysis of SnoN signaling in proliferating cells and postmitotic neurons [review]
OxyR: a molecular code for redox-related signaling.
Stamler et al., Durham, United States. In Cell, 2002
Using the transcription factor OxyR as a model, we have generated, in vitro, several stable, posttranslational modifications of the single regulatory thiol (SH), including S-NO, S-OH, and S-SG, and shown that each occurs in vivo.
TGF-beta induces assembly of a Smad2-Smurf2 ubiquitin ligase complex that targets SnoN for degradation.
Wrana et al., Toronto, Canada. In Nat Cell Biol, 2001
TGF-beta also induces the association of Smurf2 with the transcriptional co-repressor SnoN and we show that Smad2 can function to mediate this interaction.
Negative feedback regulation of TGF-beta signaling by the SnoN oncoprotein.
Luo et al., Berkeley, United States. In Science, 1999
The SnoN oncoprotein was found to interact with Smad2 and Smad4 and to repress their abilities to activate transcription through recruitment of the transcriptional corepressor N-CoR.
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