ArticleThe Journal of biological chemistry2008
Bcl-xL and UVRAG cause a monomer-dimer switch in Beclin1.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 89 citations in OpenAlex.
- Structural insights into Beclin 1 interactions with it's regulators for autophagy modulation.Computational and structural biotechnology journal · 2025Review
- Traditional Chinese medicine and its active substances reduce vascular injury in diabetes via regulating autophagic activity.Frontiers in pharmacology · 2024Review
- Suppression of non-small-cell lung cancer A549 tumor growth by an mtDNA mutation-targeting pyrrole-imidazole polyamide-triphenylphosphonium and a senolytic drug.Cancer science · 2022Article
- Review
- Bcl-xL as a Modulator of Senescence and Aging.International journal of molecular sciences · 2021Review
- The role of cell signaling in the crosstalk between autophagy and apoptosis in the regulation of tumor cell survival in response to sorafenib and neratinib.Seminars in cancer biology · 2020Review
- BCL-xL, a Mitochondrial Protein Involved in Successful Aging: FromInternational journal of molecular sciences · 2020Review
- Structural insights into BCL2 pro-survival protein interactions with the key autophagy regulator BECN1 following phosphorylation by STK4/MST1.Autophagy · 2019Article
- Post-translational modifications of Beclin 1 provide multiple strategies for autophagy regulation.Cell death and differentiation · 2019Review
- New Insights Into Beclin-1: Evolution and Pan-Malignancy Inhibitor Activity.Advances in cancer research · 2018Review
- The Autophagy-Related Beclin-1 Protein Requires the Coiled-Coil and BARA Domains To Form a Homodimer with Submicromolar Affinity.Biochemistry · 2017Article
- Regulation of the Tumor-Suppressor BECLIN 1 by Distinct Ubiquitination Cascades.International journal of molecular sciences · 2017Review
- BECN2 interacts with ATG14 through a metastable coiled-coil to mediate autophagy.Protein science : a publication of the Protein Society · 2017Article
- Activating Autophagy in Hippocampal Cells Alleviates the Morphine-Induced Memory Impairment.Molecular neurobiology · 2017Article
- Survivin inhibitor YM155 induces mitochondrial dysfunction, autophagy, DNA damage and apoptosis in Bcl-xL silenced glioma cell lines.Molecular carcinogenesis · 2017Article
- Article
- Regulation of autophagy by CaTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- Conformational flexibility of BECN1: Essential to its key role in autophagy and beyond.Protein science : a publication of the Protein Society · 2016Review
- Identification of BECN1 and ATG14 Coiled-Coil Interface Residues That Are Important for Starvation-Induced Autophagy.Biochemistry · 2016Article
- Regulation of autophagy by Beclin 1 in the heart.Journal of molecular and cellular cardiology · 2016Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Beclin1 has a key regulatory role in the initiation of autophagy and is a tumor suppressor. We have examined the interplay between viral or human Bcl-2-like proteins and UVRAG and their opposite effects on Beclin1. We show that Beclin1 forms a dimer in solution via its coiled-coil domain both in vivo and in vitro. Viral Bcl-2 binds independently to two sites on the Beclin1 dimer, one with high affinity and one with lower affinity, whereas human Bcl-x(L) binds both sites equally with relatively low affinity. UVRAG disrupts the Beclin1-dimer interface, forming a heterodimer with Beclin1, suggesting that this is how UVRAG causes its effects on Beclin1 to activate autophagy. Both Bcl-2-like proteins reduce the affinity of UVRAG for Beclin1 approximately 4-fold, suggesting that they stabilize the Beclin1 dimer. Moreover, coimmunoprecipitation assays show that UVRAG substantially reduces Beclin1 dimerization in vivo. These data explain the concentration-dependent interplay between Bcl-2, UVRAG, and Beclin1, as both tumor suppressors, UVRAG and Beclin1, have single-copy mutations in human cancers. Furthermore, our data suggest that an alternative strategy for developing anti-cancer compounds would be to disrupt the Beclin1-dimer interface.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.