Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Beclin 2 functions in autophagy, degradation of G protein-coupled receptors, and metabolism.
BECN2 interacts with ATG14 through a metastable coiled-coil to mediate autophagy.
The potent BECN2-ATG14 coiled-coil interaction is selectively critical for endolysosomal degradation of GPRASP1/GASP1-associated GPCRs.
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The BECN2 coiled-coil domain forms a heterodimer with ATG14, and this BECN2-ATG14 interaction is selectively critical for endolysosomal degradation of GPRASP1/GASP1-associated GPCRs (notably DRD2/D2R), whereas EGFR degradation depends more on BECN1-UVRAG, establishing cargo selectivity distinct from BECN1.
BECN2 (beclin 2) Negatively Regulates Inflammasome Sensors Through ATG9A-Dependent but ATG16L1- and LC3-Independent Non-Canonical Autophagy.
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BECN2 negatively regulates NLRP3, AIM2, NLRP1, and NLRC4 inflammasomes by interacting with the sensors and mediating their lysosomal degradation through a ULK1- and ATG9A-dependent, but BECN1/WIPI2/ATG16L1/LC3-independent, non-canonical autophagic pathway involving SNAREs SEC22A, STX5, and STX6.
Beclin 2 negatively regulates innate immune signaling and tumor development.
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BECN2 targets the upstream kinases MEKK3 (MAP3K3) and TAK1 (MAP3K7) for ATG9A-dependent (ATG16L/Beclin 1/LC3-independent) autophagic degradation, thereby negatively regulating ERK1/2 and NF-kB innate immune signaling; Becn2-deficient mice develop increased inflammation and lymphoma, rescued by myeloid MEKK3 ablation.
Deciphering functional roles and interplay between Beclin1 and Beclin2 in autophagosome formation and mitophagy.
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Both Beclin-1 and Beclin-2 contribute to autophagosome formation, but selective mitophagy is compromised only by Beclin-1 loss (requiring ULK1 phosphorylation of Beclin-1 Ser15 and MAM localization); Beclin-2 is not required for mitophagy, supporting reassignment of BECN2 mitophagy annotation to general autophagosome assembly.
Beclin orthologs: integrative hubs of cell signaling, membrane trafficking, and physiology.
UniProtKB record for BECN2