IndraLab

Statements

USP9X activates SMAD4. 12 / 15
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"Loss of the USP9x homologue Fat facets in Drosophila inhibits the activity of the Smad4 homologue Medea through ubiquitination of Medea on K738 (equivalent to K519 in human Smad4) (Stinchfield et al.,[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"[87] Monoubiquitination of Smad4 renders it inactive, and deubiquitination by USP9 restores Smad4 functionality and signaling."
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"USP9X was previously reported to regulate Smad4 transcriptional activity positively, thus we hypothesized that decreased USP9X expression would attenuate Smad4 function and TGF-beta responsiveness in HCC cell lines [XREF_BIBR]."
24890815
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"However, our domain truncation data indicate that activated BRK interacts with an MH1 domain of SMAD4, which does not contain the SH3 recognition motif, suggesting that the Pro-X-X-Pro motif might be dispensable for SH3-mediated protein-protein interactions.Dupont et al. (34) previously found that a cycle of ubiquitination and deubiquitination regulates the function and protein-protein interaction of SMAD4: Ecto/TIF1γ-mediated monoubiquitination disassembles SMAD4 from the SMAD complex, while deubiquitination by FAM/USP9x allows SMAD4 to return to SMAD signaling pool."
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"Thus, the de-ubiquitylase FAM and USP9 can remove K519 mono-ubiquitylation of Smad4 imposed by TIF1gamma, and thus restore Smad4 function."
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"Since USP9X was previously reported to positively regulate SMAD4 transcriptional activity 17 and SMAD4 is commonly mutated in PDA 4, we hypothesized that Usp9x loss would attenuate Smad4 function or TGFbeta responsiveness in PDA cell lines."
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"USP9x has been reported to increase SMAD4 activity by removing an inhibitory ubiquitin moiety [XREF_BIBR]."
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"A recent study reported that USP9X activates SMAD4 by deubiquitination at K519, resulting in the activation of SMAD2/3, and promotion of TGFbeta pathway, which will induce cell apoptosis."
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"During the development of PD, USP9X regulates the level of α-synuclein and activates SMAD4 by stabilizing it at K519 and subsequently promoting the TGF-β pathway (often correlated with several neurodegenerative diseases) ( xref )."
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"Sall4 shows an interaction with Usp9x (XREF_FIG B), an essential component of the TGF-beta and BMP signaling pathway, which activates Smad4 by removing a monoubiquitin group."
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"Removal of the mono-ubiquitin by the de-ubiquitinase FAM and USP9x restores Smad4 function [XREF_BIBR]."
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"3.5 USP9X targets SMAD4 for deubiquitylation in the TGFbeta pathway."
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