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Human Polyclonal SKIL Primary Antibody für 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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Human Polyclonal SKIL Primary Antibody für IHC (p), WB - ABIN541155
Derynck, Akhurst, Balmain: TGF-beta signaling in tumor suppression and cancer progression. in Nature genetics 2001
Show all 3 Pubmed References
Our results show that SnoN, and SMAD heteromers can form a joint structural core for the binding of other transcription modulators.
It is a critical negative regulator of TGF-beta1/Smad signal pathway, involving in tubule epithelial-mesenchymal transition (EMT), extracellular matrix (ECM) accumulation, and tubulointerstitial fibrosis.
signal transducer and activator of transcription (Stat)3 represses Smad3 in synergy with the potent negative regulators of TGF-beta signaling, c-Ski 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 and the subsequent phosphorylation of TAZ, leading to TAZ 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 through the TGF-b1/Smad 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 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 protein TIF1gamma promotes sumoylation of SKI-like proto-oncogene protein SnoN1 and regulates epithelial-mesenchymal transition (EMT).
The results indicate that protein ubiquitination promotes megakaryopoiesis via degrading SnoN, an inhibitor of CD61 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
these studies identify TLOC1 and SKIL as driver genes at 3q26 and more broadly suggest that cooperating genes may be coamplified in other regions with somatic copy number gain.
High SnoN expression is associated with metastasis in breast cancer.
Phospholipid Scramblase 1, an interferon-regulated gene located at 3q23, is regulated by SnoN/SkiL in ovarian cancer cells.
These data strongly suggest that SnoN can function as a tumor suppressor at early stages of tumorigenesis in human cancer tissues.
These results support our observation that cancer tissues have lower expression levels of SnoN, miR-720, and miR-1274A compared to adjacent normal tissues from esophageal squamous cell carcinoma patients.
Data suggest that SKIL expression is modulated by antineoplastic agents and may be involved in drug resistance in ovarian carcinoma; up-regulation of SKIL expression by arsenic trioxide and reduction of apoptosis involves activation of PI3K pathway.
SNON predominantly associates with SMAD2 at the promoters of primitive streak (PS) and early DE marker genes
the SNON-SMAD4 complex negatively regulated basal SKIL gene expression through binding the promoter and recruiting histone deacetylases
SnoN has been implicated in distinct aspects of the development of postmitotic neurons, this study identifies a novel function for SnoN in neuronal precursors in the mammalian brain
SnoN plays an important in vivo role in adipocyte differentiation and white adipose tissue development in vivo by decreasing activity in the activin/Smad2 signaling pathway.
Loss of SnoN is associated with partial embryonic lethality, mostly due to defects in angiogenesis in both the yolk sac 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 signaling, coordinates TGF-beta and prolactin signaling to control alveologenesis and lactogenesis.
mRNA for positive regulators of Fshb expression, such as Fos and Jun, were up-regulated at slower pulse frequencies than a number of potential negative regulators, such as the corepressors Skil, Crem, and Tgif1.
The endogenous SnoN plays a role in regulating ADAM12 expression in response to TGFbeta1.
The authors conclude that somatic and germ cells at all differentiation stages are actively transducing TGFbeta superfamily signals but that responses to these ligands may be selectively modulated by SnoN2.
Sno is a significant negative regulator of antiproliferative TGF-beta 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 induces degradation of SnoN and c-Ski in addition to Smad7.
SnoN plays an essential role in AFP repression by positively regulating mSin3A protein levels. p53 and SnoN are both needed to recruit the mSin3A corepressor.
These data indicate that SnoN is expressed in a cell-specific manner during ovarian follicular development, atresia, and luteinization and that SnoN might play essential roles in these physiological processes.
SnoN functions as a tumour suppressor by inducing premature senescence.
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