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these findings reveal a new regulatory mechanism of HSPB6 in cell survival through its interaction with BECN1.
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High beclin1 expression is associated with Glioma.
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Our data presents evidence that AEG-1, LC3-II, Beclin-1, and HIF-1alpha are significantly up-regulated in T-NHL tissues, and hypoxia triggers AEG-1, LC3-II and Beclin-1 expression in T-NHL cells.
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Paraffin-embedded tissues from 121 consecutive patients treated with surgery for gastric cancer were analyzed immunohistochemically for the expression of autophagic proteins microtubule-associated proteins 1A/1B light chain 3A and 3B (LC3A, LC3B) and beclin-1.
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Study demonstrated that the expression of Beclin 1 was upregulated in 4nitroquinoline1oxideinduced oral carcinogenesis, accompanied with myeloidderived suppressor cells and regulatory T cells accumulation.
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decreased Beclin-1 expression might relate to poor differentiation and unfavorable outcome in hepatocellular carcinoma
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BECN1knockout inhibited the migratory and invasive ability of MDAMB231 cells by partially reversing signals of epithelial-mesenchymal transition.Analysis of publicly available gene expression datasets revealed increased expression of BECN1 in triple-negative breast cancer samples.
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Low beclin 1 expression is associated with synovial sarcoma.
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ISG15 reduces miR-17-5p levels and thereby promotes Beclin-1-mediated autophagy
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CaMKII can directly phosphorylate Beclin 1 at Ser90 to promote K63-linked ubiquitination of Beclin 1 and activation of autophagy; it also promotes K63-linked ubiquitination of inhibitor of differentiation 1/2 (Id-1/2) by catalyzing phosphorylation of Id proteins and recruiting TRAF-6
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PFN1 could promote autophagy through taking part in Beclin1 complex and contribute to bortezomib resistance, which may become a novel molecular target in the therapy of MM.
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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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Silencing Beclin-1 can attenuate hypoxia-induced VM formation and the metastatic ability of U87MG cells and is a potential target for VM inhibition in glioma.
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Endogenous HER2 interacts with Beclin 1 in breast cancer cells and inhibits autophagy. BECN1 allelic loss is common and associated with a worse prognosis in patients with HER2-overexpressing breast tumors.
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To induce the redistribution of Beclin 1 among its self-associated form or Atg14L/UVRAG-containing complexes enhances both autophagy and endolysosomal trafficking.
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Phosphorylated and activated deoxycytidine kinase inhibits ionizing radiation (IR)-induced total cell death and apoptosis, and promotes IR-induced autophagy through the mTOR pathway and by inhibiting the binding of Bcl2 protein to BECN1 in breast cancer cells.
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Variation found in the BECN1 promoter modulates expression levels of this gene. Machado-Joseph Disease patients carrying the rs60221525 C allele presented a tendency for earlier estimated age at onset. Moreover, patients with the rs60221525 C allele presented a more severe clinical picture, compared to patients without this allele.
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that after Caspase 3-mediated Beclin 1 cleavage at 146/149 sites, the N-terminal fragments of Beclin 1 may partially translocate into nuclei in neurons subjected to AD-like injury
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miR-216b enhances the efficacy of vemurafenib and reverses drug resistance by targeting Beclin-1, UVRAG and ATG5 in melanoma.
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TRIM50, via the RING domain, ubiquitinates Beclin 1 in a K63-dependent manner enhancing its binding with ULK1 and autophagy activity.
