SKIL Antibody

1. 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. PMID: 28707079
2. 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 PMID: 28115165
3. 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. PMID: 27237790
4. suggest that SnoN suppresses TGF-betainduced epithelial-mesenchymal transition and invasion of bladder cancer cells in a TIF1gammadependent manner PMID: 27430247
5. 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. PMID: 26743567
6. RNAi-mediated downregulation of SnoN effectively inhibited proliferation and enhanced apoptosis of pancreatic cells. PMID: 25907906
7. 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. PMID: 25749039
8. 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 PMID: 25464936
9. Data indicate that tripartite motif containing 33 protein TIF1gamma promotes sumoylation of SKI-like proto-oncogene protein SnoN1 and regulates epithelial-mesenchymal transition (EMT). PMID: 25059663
10. The results indicate that protein ubiquitination promotes megakaryopoiesis via degrading SnoN, an inhibitor of CD61 expression, strengths the roles of ubiquitination in cellular differentiation. PMID: 24637302
11. 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 PMID: 23446947
12. 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. PMID: 23764425
13. High SnoN expression is associated with metastasis in breast cancer. PMID: 23832742
14. Phospholipid Scramblase 1, an interferon-regulated gene located at 3q23, is regulated by SnoN/SkiL in ovarian cancer cells. PMID: 23621864
15. These data strongly suggest that SnoN can function as a tumor suppressor at early stages of tumorigenesis in human cancer tissues. PMID: 23418461
16. 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. PMID: 23154181
17. 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. PMID: 23178716
18. SNON predominantly associates with SMAD2 at the promoters of primitive streak (PS) and early DE marker genes PMID: 23154981
19. the SNON-SMAD4 complex negatively regulated basal SKIL gene expression through binding the promoter and recruiting histone deacetylases PMID: 22674574
20. SnoN mediates a negative feedback mechanism evoked by TGF-beta to inhibit BMP signaling and, subsequently, hypertrophic maturation of chondrocytes. PMID: 22767605
21. SnoN may have broad functions in the embryonic development and tissue morphogenesis [Review] PMID: 22710172
22. analysis of SnoN signaling in proliferating cells and postmitotic neurons [review] PMID: 22710173
23. SnoN level promotes ERalpha signaling and possibly breast cancer progression. PMID: 22227247
24. The flexibility in the putative protein binding groove enables SnoN to recognize multiple interaction partners. PMID: 20957027
25. Regulation of TGF-beta-co-repressor (SnoN) is greatly affected suggesting that SnoN as a cardinal player in cholestasis-induced fibrogenesis. PMID: 19889106
26. The endogenous SnoN plays a role in regulating ADAM12 expression in response to TGFbeta1. PMID: 20457602
27. SnoN elevation is associated with mammary gland branching morphogenesis, postlactational involution, and mammary tumorigenesis. PMID: 20460516
28. BMP-7 prevents TGF-beta-mediated loss of the transcriptional repressor SnoN and hence specifically limits Smad3 DNA binding. PMID: 20093492
29. Inhibition of Smad signaling may be achieved at the transcriptional level through c-Ski/receptor-Smad/co-mediator Smad4 interactions--REVIEW PMID: 19898560
30. SnoN acts as a positive mediator of TGF-beta-induced transcription and cell cycle arrest in lung epithelial cells PMID: 15677458
31. Sno expression was identified as an important mechanism to shut off antiproliferative TGF-beta signaling in malignant melanoma PMID: 15809735
32. mechanism of regulation of TGF-beta signaling via differential subcellular localization of SnoN PMID: 16109768
33. A novel role of SnoN in the transforming activity of TGF-beta in fibroblasts was demonstrated. PMID: 16314499
34. SnoN also seems to regulate negatively the TGF-beta-responsive SMAD, mothers against DPP homolog 7 gene by binding and repressing its promoter in a similar way to Ski PMID: 16442497
35. SnoN is directly regulated by sumoylation leading to the enhancement of the ability of SnoN to repress transcription in a promoter-specific manner PMID: 16966324
36. snoN protein has both oncogenic and tumor suppressive properties in colorectal tumorigenesis. PMID: 17062133
37. SnoN plays both pro-tumorigenic and antitumorigenic roles at different stages of mammalian malignant progression PMID: 17074815
38. Arkadia induces degradation of SnoN and c-Ski in addition to Smad7. PMID: 17510063
39. Results show that Arkadia specifically activates transcription via Smad3/Smad4 binding sites by inducing degradation of the transcriptional repressor SnoN. PMID: 17591695
40. CREB activation, in concert with Sp1, constitutes a molecular switch that confers the cell type-specific induction of SnoN in response to HGF stimulation PMID: 17625116
41. SnoN overexpression is associated with depth of invasion and recurrence in patients with esophageal squamous cell carcinoma. PMID: 18612694
42. Data show that dominant-negative transforming growth factor beta type II receptor decreases matrix metalloproteinase 2 in hepatic stellate cells, and upregulates SKI-like oncogene, which antagonizes TGF-beta signaling. PMID: 19189315
43. results implicate SnoN levels in multiple roles during ovarian carcinogenesis: promoting cellular proliferation in ovarian cancer cells and as a positive mediator of cell cycle arrest and senescence in non-transformed ovarian epithelial cells PMID: 19383336
44. SnoN is involved in differentiation in normal skin and benign and nonmetastatic skin tumors, but plays a proto-oncogenic role in undifferentiated squamous cell carcinoma PMID: 19538364

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HGNC: 10897

OMIM: 165340

KEGG: hsa:6498

STRING: 9606.ENSP00000259119

UniGene: Hs.536655