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抗Rat (Rattus) 抗体:
抗Mouse (Murine) 抗体:
Human Polyclonal SKIL Primary Antibody for IHC, ELISA - ABIN1003171
Li, Turck, Teumer, Stavnezer: Unique sequence, ski, in Sloan-Kettering avian retroviruses with properties of a new cell-derived oncogene. in Journal of virology 1986
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It is a critical negative regulator of TGF-beta1 (显示 TGFB1 抗体)/Smad (显示 SMAD1 抗体) signal pathway, involving in tubule epithelial-mesenchymal transition (EMT (显示 ITK 抗体)), extracellular matrix (ECM (显示 MMRN1 抗体)) accumulation, and tubulointerstitial fibrosis.
signal transducer and activator of transcription (Stat (显示 STAT1 抗体))3 (显示 STAT3 抗体) represses Smad3 (显示 SMAD3 抗体) in synergy with the potent negative regulators of TGF-beta (显示 TGFB1 抗体) signaling, c-Ski (显示 SKI 抗体) 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 (显示 TAZ 抗体) and the subsequent phosphorylation of TAZ (显示 TAZ 抗体), leading to TAZ (显示 TAZ 抗体) 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 (显示 SMURF2 抗体) through the TGF-b1/Smad (显示 SMAD1 抗体) 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 (显示 PCSK1 抗体) 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 (显示 TRIM33 抗体) protein TIF1gamma (显示 TRIM33 抗体) promotes sumoylation of SKI-like proto-oncogene (显示 RAB1A 抗体) protein SnoN1 and regulates epithelial-mesenchymal transition (EMT (显示 ITK 抗体)).
The results indicate that protein ubiquitination promotes megakaryopoiesis via degrading SnoN, an inhibitor of CD61 (显示 ITGB3 抗体) expression, strengths the roles of ubiquitination in cellular differentiation.
Loss of SnoN is associated with partial embryonic lethality, mostly due to defects in angiogenesis in both the yolk sac (显示 ADCY10 抗体) 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 (显示 TGFB1 抗体) signaling, coordinates TGF-beta (显示 TGFB1 抗体) and prolactin (显示 PRL 抗体) signaling to control alveologenesis and lactogenesis.
mRNA for positive regulators of Fshb (显示 FSHB 抗体) expression, such as Fos and Jun (显示 JUN 抗体), were up-regulated at slower pulse frequencies than a number of potential negative regulators, such as the corepressors Skil, Crem (显示 CREM 抗体), and Tgif1 (显示 TGIF1 抗体).
The endogenous SnoN plays a role in regulating ADAM12 (显示 ADAM12 抗体) expression in response to TGFbeta1 (显示 TGFB1 抗体).
The authors conclude that somatic and germ cells at all differentiation stages are actively transducing TGFbeta (显示 TGFB1 抗体) superfamily signals but that responses to these ligands may be selectively modulated by SnoN2.
Sno (显示 SBNO2 抗体) is a significant negative regulator of antiproliferative TGF-beta (显示 TGFB1 抗体) 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 (显示 RNF111 抗体) induces degradation of SnoN and c-Ski (显示 SKI 抗体) in addition to Smad7 (显示 SMAD7 抗体).
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-related oncogene snoN
, ski/sno related
, SKI-like oncogene
, v-ski sarcoma viral oncogene homolog
, Ski-like protein
, ski-like protein-like
, ski-related oncogene
, LOW QUALITY PROTEIN: ski-like protein
, SKI-like oncogene b