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LC3 may influence the perineural invasion and prognosis of pancreatic cancer through ubiquitin C
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p66SHC is a novel regulator of autophagy and mitophagy in B cells and recruits LC3-II. This implies p66SHC-mediated coordination of autophagy and apoptosis in B cell survival and differentiation.
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LC3 and STRAP regulate actin filament assembly by JMY during autophagosome formation.
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Data reveal that the stability and cargo recognition ability of LC3 are highly dependent on its acetylation. Acetylation blocked LC3's interaction with p62 preventing the mis-targeting of p62 to nonautophagic LC3 and thus permitting the efficient degradation of autophagic cargoes. Acetylation also inhibited LC3 proteasome-dependent degradation, thus maintaining LC3 as a long-lived protein that could be used as a reserve.
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Flightless-I functions as a checkpoint protein for selective autophagy by interacting with p62 to block its recognition of LC3, leading to tumorigenesis in breast cancer.
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Data reveal the nuanced role of the ATG14 ALPS in membrane curvature sensing, suggesting that the ALPS has additional roles in supporting LC3 lipidation.
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A new molecular mechanism has been described in uterine sarcoma, by which miR-152 and miR-24 promote autophagy by activating SIRT1 and deacetylating LC3.
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PHB2 forms a ternary protein complex with sequestosome 1 (SQSTM1) and LC3, leading to loading of LC3 onto the damaged mitochondria.
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The distribution of nuclear LC3 can be a novel way for further studying death of acute myeloid leukemia (AML) cells,and the regulatory molecules may be new targets for treating AML.
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calreticulin induces autophagy by interacting with microtubule-associated protein 1A/1B-light chain 3 (LC3). Confocal microscopy revealed that the colocalization of calreticulin and LC3 at the autophagosome was enhanced under ER stress conditions.
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High expression of LC3, beclin 1 and p62 was significantly more frequent in high-grade gliomas than in low-grade.Kaplan-Meier analyses revealed that LC3, p62 and autophagy status were significantly associated with poorer survival.
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These results unambiguously demonstrate that IcsB is required for double-membrane vacuole escape during cell-to-cell spread, regardless of LC3 recruitment, and do not support the previously proposed notion that autophagy counters Shigella flexneri dissemination.
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Absence of MAP1LC3A disrupts the autophagic pathway and leads to the failure of aggresome vimentin cage degradation in primary choroid plexus carcinoma.
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High LC3 expression is associated with Glioma.
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Intense autophagic activity, as assessed by LC3A immunostaining and Stone-like structures quantification, is a strong prognostic marker in gastric cancer and can be useful for clinical application.
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show that the WD repeat-containing C-terminal domain (WD40 CTD) of ATG16L1 is essential for LC3 recruitment to endolysosomal membranes during non-canonical autophagy
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Expression and Clinical Significance of LC-3 and P62 in Non-small Cell Lung Cancer
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The results suggest that autophagy-associated proteins LC3A, LC3B, and Beclin-1 might be potential biomarkers for subclassification, differentiation, and local metastasis in primary lung tumor.
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High LC3 Expression is Associated with Cancer Progression and Chemo-Resistance in Esophageal Squamous Cell Carcinoma.
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Data suggest that, in patients with diabetic kidney disease, urinary excretion of mRNAs for MAP1LC3A, WIPI2, and RB1CC1 is down-regulated as compared to healthy control subjects; these transcripts may serve as urinary autophagy biomarkers. (MAP1LC3A = microtubule associated protein 1 light chain 3; WIPI2 = WD repeat domain phosphoinositide-interacting protein 2; RB1CC1 = RB1 inducible coiled-coil 1)