IndraLab

Statements

CYLD inhibits AKT. 12 / 26
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"Overexpression of CYLD, a DUB for K63 linked ubiquitination of AKT, decreases AKT activity mediated by TRAF6 [XREF_BIBR]."
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"Thus, we next explored the possibility that CYLD may inhibit Akt mediated fibrotic response via deubiquitinating TRAF6."
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"In search of underlying molecular mechanisms, we find that CYLD knockout mice display marked overactivation of Akt and mTOR and reduced autophagic flux, and conversely, CYLD overexpression potently suppresses Akt and mTOR activity and promotes autophagy."
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"On the other hand, the deubiquitinating enzyme CYLD and ubiquitin specific peptidase 1 can remove K63-linked polyubiquitin chains on Akt and then inhibit Akt activation [105, 106]."
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"Taken together, these data provide strong evidence that CYLD negatively regulates Akt by directly interacting with and deubiquitinating K63 polyubiquitinated Akt, both in vitro in a cell-free system and in vivo under endogenous condition."
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"The results indicated that lncRNA CRAL could sponge miRNA-505 to upregulate the cylindromatosis gene (CYLD) expression, which subsequently inhibited AKT activation and resulted in an enhancement in the sensitivity of GC cells to DDP 71."
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"To further determine how CYLD negatively regulates Akt, we first examined whether CYLD physically interacts with Akt by performing co-immunoprecipitation experiments."
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"Furthermore, the results indicated that CRAL mainly resided in the cytoplasm and could sponge endogenous miR-505 to upregulate cylindromatosis (CYLD) expression, which further suppressed AKT activation and led to an increase in the sensitivity of gastric cancer cells to cisplatin in vitro and in preclinical models."
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"These results suggest that CYLD suppresses Akt activation to inhibit prostate cancer cells growth and development."
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"Nonetheless, these data demonstrate that CYLD indeed inhibits Akt mediated fibrotic response by at least in part directly interacting with and deubiquitinating Akt."
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"It is possible that CYLD may inhibit Akt mediated fibrotic response by actually deubiquitinating TRAF6."
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"As shown in XREF_SUPPLEMENTARY, CYLD knockdown, using siCYLD, still enhanced TGF-beta-induced fibrotic response in TRAF6 depleted cells, thereby suggesting that CYLD inhibits Akt mediated fibrotic response at least in part by directly interacting with and deubiquitinating Akt."
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