Virus-encoded proteases play diverse roles in the efficient replication of enterovirus 71 (EV71) which is the causative agent of human hand foot and mouth disease (HFMD). ATG4B protein processes the viral polyprotein with its cysteine protease activity and helps EV71 replicate through a chemical biology strategy.
Autophagy-related 4 cysteine peptidase (ATG4) proteases process inactive pro-LC3/GABARAP before lipidation and the same proteases can also deconjugate LC3/GABARAP from lipids.
ERBB2 might modulate ATG4B for autophagy induction in oxidative stress-stimulated ARPE-19 cells. ERBB2 knockdown also caused an accumulation of nuclear factor erythroid 2-related factor 2 (NRF2) and enhanced its transcriptional activity.
Human HAP1 and HeLa cells lacking ATG4B exhibit a severe but incomplete defect in LC3/GABARAP processing and autophagy. By further genetic depletion of ATG4 isoforms using CRISPR-Cas9 and siRNA we uncover that ATG4A ATG4C and ATGD all contribute to residual priming activity which is sufficient to enable lipidation of endogenous GABARAPL1 on autophagic structures.
our results demonstrated that the interaction of Atg4B and Bcl-2 might play an important role in Cd-induced crosstalk between apoptosis and autophagy through disassociation of Bcl-2-Beclin1. Cd-induced autophagy is apoptosis-dependent and prevents apoptotic cell death to ensure the growth and proliferation of A549 cells.
that the phosphorylation of ATG4B at Ser34 participates in the metabolic reprogramming of hepatocellular carcinoma cells via repressing mitochondrial function
ATG4B expression was observed markedly upregulated by EWS-FLI1 overexpression and silencing of ATG4B dramatically inhibits autophagy in Ewing sarcoma cells.
Reporter assay showed that HSF1 increased the transcriptional activity of ATG4B gene promoter and chromatin immunoprecipitation assay verified that HSF1 bound to the site (-1429 to -1417) in ATG4B gene promoter region.
study demonstrates that Rab7b regulates LC3 processing by modulating Atg4B activity; taken together findings reveal Rab7b as a novel negative regulator of autophagy through its interaction with Atg4B
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