IndraLab

Statements

USP29 binds ACSL5. 18 / 18
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"Thus, targeting USP29-ACSL5 may constitute an effective therapeutic strategy for MASLD."
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"Moreover, USP29 directly interacted with ACSL5 and stabilized ACSL5 via K48-linked deubiquitination."
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"Furthermore, we found that USP29 directly interacted with ACSL5 and upregulated ACSL5 expression."
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"First, the interaction between USP29 and ACSL5 was further confirmed by co-IP (Fig. 7A, B)."
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"Additionally, a GST pull-down assay revealed a direct interaction between USP29 and ACSL5 (Fig. 7C, D)."
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"USP29 interacts with ACSL5 and upregulates ACSL5 expression."
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"A recent study showed that ubiquitin-specific protease 29 (USP29) acts as a protective factor against metabolic dysfunction-associated steatotic liver disease (MASLD) progression by stabilizing long-chain acyl-CoA synthase 5 (ACSL5) and enhancing fatty acid β-oxidation, suggesting that the activation of the USP29–ACSL5 axis could represent a promising therapeutic strategy for MASLD [ xref ]."
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"USP29 directly interacts with ACSL5 and stabilizes ACSL5 through the suppression of K48-linked ubiquitination."
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"First, the interaction between USP29 and ACSL5 was further confirmed by co-IP ( xref , xref )."
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"Additionally, a GST pull-down assay revealed a direct interaction between USP29 and ACSL5 ( xref , xref )."
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"The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD."
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"Moreover, USP29 directly interacted with ACSL5 and stabilized ACSL5 via K48-linked deubiquitination."
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"These findings suggest that activating USP29-ACSL5 might be a promising therapeutic approach for MASLD."
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"Together, in the present study, the regulatory effect of USP29-ACSL5 on the expression of genes involved in FAO may have occurred because, under metabolic stimulation, USP29 stabilized ACSL5 expression to promote the activation of fatty acids, which in turn activated PPARa to induce the expression of genes involved in FAO and then directed them to the mitochondria for β-oxidation."
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