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.
study elucidated a novel Malat1-miR-101-STMN1/RAB5A/ATG4D regulatory network that Malat1 activates autophagy and promotes cell proliferation by sponging miR-101 and upregulating STMN1 RAB5A and ATG4D expression in glioma cells
This study highlights the transcriptional inactivation mechanisms of ATG2B ATG4D ATG9A and ATG9B promoter methylation status and the possible origin of autophagy signal pathway repression in invasive ductal carcinomas.
The actions of ATG4 family members (particularly ATG4B) are required for the control of autophagosome fusion with late degradative compartments in differentiating human erythroblasts.
the import of Atg4D during cellular stress and differentiation may play important roles in the regulation of mitochondrial physiology reactive oxygen species mitophagy and cell viability.
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