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FLASH GENE
Symbol MAP1LC3A contributors: mct - updated : 01-10-2016
HGNC name microtubule-associated protein 1 light chain 3 alpha
HGNC id 6838
EXPRESSION
Type widely
constitutive of
   expressed in (based on citations)
organ(s)
SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
Digestivepharynx   highly
Nervousnerve   highly
Visualeye   highly
cell lineage
cell lines
fluid/secretion
at STAGE
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • produced by the proteolytic cleavage after the conserved C-terminal Gly residue
  • HOMOLOGY
    interspecies ortholog to rat Map1lc3
    Homologene
    FAMILY GABARAP subfamily
    CATEGORY structural protein
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm,cytosolic,vesicle
    intracellular,cytoplasm,cytoskeleton,microtubule
    basic FUNCTION
  • plays an essential role in autophagy, which is involved in the bulk degradation of cytoplasmic components by the lysosomal system
  • may play a role in breast cancer development
  • role in the regulation of Rho signaling and in the reorganization of the actin cytoskeleton
  • microtubule-associated protein light chain 3, specific autophagic marker in mammalian cells, that is processed from the cytosolic form (LC3-I) to the membrane-bound form (LC3-II)
  • with MAP1LC3B, are involved in elongation of the phagophore membrane whereas the GABARAP/GABARAPL2 subfamily is essential for a later stage in autophagosome maturation
  • MAP1LC3A and MAP1LC3B and GABARAPs are essential for autophagosome formation and therefore suggest a dual role for individual members of this protein family
  • involved in the lipid droplet formation regardless of the bulk degradation, and has two pivotal roles in cellular homeostasis mediated by autophagy and lipid metabolism
  • with SLC30A4, MAP1LC3A and CASP3 might play a role in the pathophysiology of recurrent neonatal seizure-induced acute and long-term brain damage
  • modulation of MAP1LC3A levels through inhibition of histone deacetylation at the MAP1LC3A locus may be a viable option to increase basal autophagy in nondividing terminally differentiated cells
  • important role of ATG8 homologues may be to act as a scaffold for the assembly of autophagy complexes
  • GABARAP, GABARAPL1, GABARAPL2, MAP1LC3A, MAP1LC3B, are not essential for autophagosome formation but are critical for autophagosome-lysosome fusion
  • novel roles for FKBP8 and MAP1LC3A, which act together to induce mitophagy
  • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • interacting with FOXO3 (FOXO3 controls the transcription of autophagy-related genes, including MAP1LC3 and BNIP3
  • MAP1LC3A is a novel regulatory protein interacting with AKAP13
  • FYCO1 binds to both MAP1LC3A, PtdIns(3)P and RAB7A, and contains a domain responsible for microtubule plus end-dependent transport
  • MAP1S isoforms may act as a linker to bridge autophagy components not only with the microtubular cytoskeleton through interacting with MAP1LC3A isoforms, but also directly to mitochondria
  • hypoxia induced dephosphorylation of FUNDC1 and enhanced its interaction with MAP1LC3A for selective mitophagy
  • strong evidence that transcriptional repression plays a major role in regulating Atg8/LC3 levels, and this up-regulation results in an increase in the size of the autophagosome
  • ULK1 interacted most strongly with GABARAP and GABARAPL1, but it also interacted with GABARAPL2, MAP1LC3A, and MAP1LC3C
  • although AP2 and PICALM bind to MAP1LC3A, they do not seem to be direct substrates of autophagy
  • interaction between MAP1LC3A and AP2M1 as well as PICALM showed a significant increase triggered by starvation
  • at mitochondria, ULK1 interacts with FUNDC1, phosphorylating it at serine 17, which enhances FUNDC1 binding to MAP1LC3A
  • DACT1 increases autophagosome formation as indicated by elevated puncta formation of MAP1LC3A, ATG14 and ZFYVE1 (Double FYVE-containing protein 1)
  • LRPPRC interacts with MAP1S that interacts with MAP1LC3A and bridges autophagy components with microtubules and mitochondria to affect autophagy flux
  • AMBRA1 is able to induce mitophagy via MAP1LC3A binding, regardless of PARK2 and SQSTM1
  • autophagy protein MAP1LC3A/Atg8 directly interacts with the nuclear lamina protein LMNB1 (lamin B1), and binds to LMN/lamin-associated chromatin domains (LADs)
  • FUNDC1, mediate selective removal of damaged or superfluous mitochondria through their specific interaction with MAP1LC3A
  • GABARAP subfamily members, GABARAP, GABARAPL1, GABARAPL2, MAP1LC3A, MAP1LC3B, are primary contributors to PINK1/Parkin mitophagy and starvation autophagy
  • KLC1 may potentially compete with MAP1LC3A, a key component for autophagosome formation, to interact with FUNDC1
  • FKBP8 efficiently recruits lipidated MAP1LC3A to damaged mitochondria in a LIR-dependent manner
  • cell & other
    REGULATION
    ASSOCIATED DISORDERS
    ANIMAL & CELL MODELS