Normal function · from ai-gene-review (Q14457, commit 79fe13b38970) · AI-generated, not KB evidence

Beclin-1 is the central scaffold subunit of class III phosphatidylinositol 3-kinase (PI3KC3/VPS34) complexes that generate phosphatidylinositol 3-phosphate (PI3P) for autophagosome biogenesis and endocytic trafficking. BECN1 forms two mutually exclusive complexes: PI3KC3-C1 (with ATG14L) for autophagosome nucleation, and PI3KC3-C2 (with UVRAG) for endosome maturation and endocytic trafficking. The protein contains an N-terminal BH3 domain (aa 108-127) that binds BCL2/BCL-XL to regulate autophagy, a coiled-coil domain (CCD; aa 144-269) for dimerization and partner binding, and a C-terminal BARA/ECD membrane-binding domain. BECN1 is a haploinsufficient tumor suppressor and is essential for autophagy initiation through its adapter function in assembling PI3KC3 complex components.

BECN1 is the central scaffold/adapter of PI3KC3 complexes, assembling VPS34, VPS15, and complex-specific subunits (ATG14L or UVRAG) into functional lipid kinase complexes that generate PI3P for autophagy and endocytic trafficking. As scaffold of PI3KC3-C1 (ATG14L-containing complex), BECN1 is essential for autophagosome nucleation.
BECN1 directly binds VPS34 (PIK3C3), the catalytic subunit of class III PI3K, through its coiled-coil and BARA domains. This binding is essential for PI3KC3 complex formation and function.
In the knowledge base · computed from kb/ at build time

Disorders

Relationship is the entry's genetic[].relationship_type. untyped means the entry has a genetic record for the gene but does not type it; its free-text association is shown instead.

DisorderRelationshipWhere the gene appears
Ischemic Stroke no genetic record
mechanism: Post-Ischemic Autophagic-Lysosomal Dysfunction
Multiple Sclerosis no genetic record
mechanism: Oligodendrocyte Precursor and Microglial Autophagic-Mitophagic Dysregulation
Mechanism modules · computed from kb/

Identity from HGNC (snapshot 2026-10-01). Page layers are described in the gene pages documentation.