| Description | This entry represents the SKI/SnoN family of proteins, which are the products of the oncogenic sno gene. This gene was identified based on its homology to v-ski, the transforming component of the Sloan-Kettering virus. Both Ski and SnoN are potent negative regulators of TGF-beta [ ]. Overexpression of Ski or SnoN results in oncogenic transformation of avian fibroblasts; however it may also result in terminal differentiation and therefore the Ski/SnoN mechanism of action is thought to be complex [].These proteins do not have catalytic or DNA-binding activity and therefore function primarily through interaction with other proteins, acting as transcriptional cofactors. Despite their lack of DNA-binding ability, their primary function is related to transcriptional regulation, in particular the negative regulation of TGF-beta signalling [ , ]. Ski/SnoN interact concurrently with co-Smad and R-Smad and in doing so block the ability of the Smad complexes to activate transcription of the TGF-beta target genes []. Binding of Ski/SnoN may additionally stabilise the Smad heteromer on DNA, therefore preventing further binding of active Smad complexes []. As Smad complexes critically mediate the inhibitory signals of TGF-beta in epithelial cells, high levels of SKI/SnoN may promote cell proliferation. They repress gene transcription recruiting diverse corepressors and histone deacetylases and stablish cross-regulatory mechanisms with TGF-beta/Smad pathway that control the magnitude and duration of TGF-beta signals. The alteration in regulatory processes may lead to disease development [].High levels of SnoN have been shown to stabilise p53 with a resultant increase in premature senescence. SnoN interacts with the PML protein and is then recruited to the PML nuclear bodies, resulting in stabilisation of p53 and premature senescence [ ]. | Name | Transcription regulator SKI/SnoN |
| Short Name | Tscrpt_reg_SKI_SnoN | Type | Family |
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