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Loss of SnoN is associated with partial embryonic lethality, mostly due to defects in angiogenesis in both the yolk sac (show ADCY10 Proteins) and embryo body
SnoN mediates a negative feedback mechanism evoked by TGF-beta to inhibit BMP signaling and, subsequently, hypertrophic maturation of chondrocytes.
SnoN, a negative regulator of TGF-beta (show TGFB1 Proteins) signaling, coordinates TGF-beta (show TGFB1 Proteins) and prolactin (show PRL Proteins) signaling to control alveologenesis and lactogenesis.
mRNA for positive regulators of Fshb (show FSHB Proteins) expression, such as Fos and Jun (show JUN Proteins), were up-regulated at slower pulse frequencies than a number of potential negative regulators, such as the corepressors Skil, Crem (show CREM Proteins), and Tgif1 (show TGIF1 Proteins).
The endogenous SnoN plays a role in regulating ADAM12 (show ADAM12 Proteins) expression in response to TGFbeta1 (show TGFB1 Proteins).
The authors conclude that somatic and germ cells at all differentiation stages are actively transducing TGFbeta (show TGFB1 Proteins) superfamily signals but that responses to these ligands may be selectively modulated by SnoN2.
Sno is a significant negative regulator of antiproliferative TGF-beta (show TGFB1 Proteins) signaling in both T cells and other cell types in vivo
SnoN is directly regulated by sumoylation leading to the enhancement of the ability of SnoN to repress transcription in a promoter-specific manner
SnoN plays both pro-tumorigenic and antitumorigenic roles at different stages of mammalian malignant progression
Arkadia (show RNF111 Proteins) induces degradation of SnoN and c-Ski (show SKI Proteins) in addition to Smad7 (show SMAD7 Proteins).
signal transducer and activator of transcription (Stat (show STAT1 Proteins))3 (show STAT3 Proteins) represses Smad3 (show SMAD3 Proteins) in synergy with the potent negative regulators of TGF-beta (show TGFB1 Proteins) signaling, c-Ski (show SKI Proteins) and SnoN, whereby renders gefitinib-sensitive HCC827 cells resistant
SnoN interacts with multiple components of the Hippo pathway to inhibit the binding of Lats2 to TAZ (show TAZ Proteins) and the subsequent phosphorylation of TAZ (show TAZ Proteins), leading to TAZ (show TAZ Proteins) stabilization.
suggest that SnoN suppresses TGF-betainduced epithelial-mesenchymal transition and invasion of bladder cancer cells in a TIF1gammadependent manner
the findings of this study demonstrate that the downregulation of SnoN expression in hRPTECs under high-glucose conditions is mediated by the increased expression of Smurf2 (show SMURF2 Proteins) through the TGF-b1/Smad (show SMAD1 Proteins) signaling pathway.
RNAi-mediated downregulation of SnoN effectively inhibited proliferation and enhanced apoptosis of pancreatic cells.
SKIL knockdown led to growth arrest in PC-3 (show PCSK1 Proteins) and LNCaP cell line models of prostate cancer, and its overexpression led to increased invasiveness in RWPE-1 cells.
Whole exome sequencing of the blood of the patient and both parents revealed a de novo germline SKIL mutation in the child that was not present in either parent
Data indicate that tripartite motif containing 33 (show TRIM33 Proteins) protein TIF1gamma (show TRIM33 Proteins) promotes sumoylation of SKI-like proto-oncogene (show RAB1A Proteins) protein SnoN1 and regulates epithelial-mesenchymal transition (EMT (show ITK Proteins)).
The results indicate that protein ubiquitination promotes megakaryopoiesis via degrading SnoN, an inhibitor of CD61 (show ITGB3 Proteins) expression, strengths the roles of ubiquitination in cellular differentiation.
SnoNspecific siRNA is capable of effectively inhibiting the expression of SnoN in human HepG2 cells, and the downregulation of SnoN expression induces growth inhibition and apoptosis
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.
, Ski-like protein
, ski-like protein-like
, ski-like protein
, ski-related oncogene
, ski/sno related
, ski-related oncogene snoN
, v-ski sarcoma viral oncogene homolog