IndraLab

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USP9X activates TGFB. 13 / 14
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"These results indicate that FAM induce mesangial-to-myofibroblast differentiation and promote the enlargement of the DKD fibrotic niche by activating the TGF-β /Smad2/3/YAP signal axis (Fig. 4M)."
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"USP9X positively regulates TGF-beta signaling by deubiquitylating SMAD4 and promoting its association with SMAD2 [XREF_BIBR]."
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"USP9X might also act as a regulator of the TGF-beta pathway, another signaling circuitry of great relevance to cancer, as witnessed by the fact that loss of USP9X abolishes multiple TGF-beta gene responses XREF_BIBR."
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"The deubiquitylating enzyme USP9X (also known as FAM) reverts the effects of TRIM33 on Smad4 and restores TGF-beta signaling."
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"FAM and USP9x activity is required for Smad4 mediated TGFbeta signaling, because it re-enables Smad4 to form complexes with R-Smads and signal in the nucleus."
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"The results, exemplified in Figures 1 C, 1D, and S1, show that loss of FAM abolishes multiple TGFbeta gene responses."
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"FAM knockdown also blocks TGFbeta mediated induction of a synthetic Smad promoter fused to luciferase (CAGA12-lux, Figure 1 E), in line with the notion that FAM is a critical factor for Smad signaling[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Thus, USP9X may mediate the function of TGF-β1 on promoting CSCs occurrence and EMT transition in vitro.In vivo, orthotopic tumor models were established via injecting the luciferase-expressing ID8 cells (ID8-luc) into the ovarian bursal cavity of C57BL/6 mice and visualized with Caliper IVIS Spectrum System."
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"Thus , USP9X activates TGF-beta signaling by antagonizing Smad4 monoubiquitination ( Dupont et al ., 2009 ) ."
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"Functionally and molecularly, these data indicate that USP9X mediates TGF-β function in promoting drug resistance in HGOSC, via maintaining CSCs."
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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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"Loss of Usp9x Disrupts Cortical Architecture, Hippocampal Development and TGFbeta Mediated Axonogenesis."
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"Furthermore, the positive regulator of TGF-β signaling USP9x is a candidate substrate of MIB1 [ 10 , 31 ]."
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