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Loss of SnoN is associated with partial embryonic lethality, mostly due to defects in angiogenesis in both the yolk sac (zeige ADCY10 Proteine) 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 (zeige TGFB1 Proteine) signaling, coordinates TGF-beta (zeige TGFB1 Proteine) and prolactin (zeige PRL Proteine) signaling to control alveologenesis and lactogenesis.
mRNA for positive regulators of Fshb (zeige FSHB Proteine) expression, such as Fos and Jun (zeige JUN Proteine), were up-regulated at slower pulse frequencies than a number of potential negative regulators, such as the corepressors Skil, Crem (zeige CREM Proteine), and Tgif1 (zeige TGIF1 Proteine).
The endogenous SnoN plays a role in regulating ADAM12 (zeige ADAM12 Proteine) expression in response to TGFbeta1 (zeige TGFB1 Proteine).
The authors conclude that somatic and germ cells at all differentiation stages are actively transducing TGFbeta (zeige TGFB1 Proteine) superfamily signals but that responses to these ligands may be selectively modulated by SnoN2.
Sno is a significant negative regulator of antiproliferative TGF-beta (zeige TGFB1 Proteine) 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 (zeige RNF111 Proteine) induces degradation of SnoN and c-Ski (zeige SKI Proteine) in addition to Smad7 (zeige SMAD7 Proteine).
signal transducer and activator of transcription (Stat (zeige STAT1 Proteine))3 (zeige STAT3 Proteine) represses Smad3 (zeige SMAD3 Proteine) in synergy with the potent negative regulators of TGF-beta (zeige TGFB1 Proteine) signaling, c-Ski (zeige SKI Proteine) 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 (zeige TAZ Proteine) and the subsequent phosphorylation of TAZ (zeige TAZ Proteine), leading to TAZ (zeige TAZ Proteine) 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 (zeige SMURF2 Proteine) through the TGF-b1/Smad (zeige SMAD1 Proteine) 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 (zeige PCSK1 Proteine) 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 (zeige TRIM33 Proteine) protein TIF1gamma (zeige TRIM33 Proteine) promotes sumoylation of SKI-like proto-oncogene (zeige RAB1A Proteine) protein SnoN1 and regulates epithelial-mesenchymal transition (EMT (zeige ITK Proteine)).
The results indicate that protein ubiquitination promotes megakaryopoiesis via degrading SnoN, an inhibitor of CD61 (zeige ITGB3 Proteine) 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