MAP1LC3B

The product of this gene is a subunit of neuronal microtubule-associated MAP1A and MAP1B proteins, which are involved in microtubule assembly and important for neurogenesis. Studies on the rat homolog implicate a role for this gene in autophagy, a process that involves the bulk degradation of cytoplasmic component.

Microtubule Associated Protein 1 Light Chain 3 Beta

LC3B; ATG8F; MAP1LC3B-a; MAP1A/1BLC3

Ubiquitin-like modifier involved in formation of autophagosomal vacuoles (autophagosomes) (PubMed:20418806, PubMed:23209295, PubMed:28017329).
Plays a role in mitophagy which contributes to regulate mitochondrial quantity and quality by eliminating the mitochondria to a basal level to fulfill cellular energy requirements and preventing excess ROS production (PubMed:23209295, PubMed:28017329).
In response to cellular stress and upon mitochondria fission, binds C-18 ceramides and anchors autophagolysosomes to outer mitochondrial membranes to eliminate damaged mitochondria (PubMed:22922758).
While LC3s are involved in elongation of the phagophore membrane, the GABARAP/GATE-16 subfamily is essential for a later stage in autophagosome maturation (PubMed:20418806, PubMed:23209295, PubMed:28017329).
Promotes primary ciliogenesis by removing OFD1 from centriolar satellites via the autophagic pathway (PubMed:24089205).
Through its interaction with the reticulophagy receptor TEX264, participates in the remodeling of subdomains of the endoplasmic reticulum into autophagosomes upon nutrient stress, which then fuse with lysosomes for endoplasmic reticulum turnover (PubMed:31006537, PubMed:31006538).
Upon nutrient stress, directly recruits cofactor JMY to the phagophore membrane surfaces and promotes JMY's actin nucleation activity and autophagosome biogenesis during autophagy (PubMed:30420355).

Autophagosome assemblyManual Assertion Based On ExperimentIBA:GO_Central
Autophagosome maturationManual Assertion Based On ExperimentIDA:UniProtKB
AutophagyManual Assertion Based On ExperimentIDA:CAFA
Autophagy of mitochondrionManual Assertion Based On ExperimentIGI:ParkinsonsUK-UCL
Cellular response to nitrogen starvationManual Assertion Based On ExperimentIBA:GO_Central
Cellular response to starvationManual Assertion Based On ExperimentIDA:UniProtKB
MacroautophagyManual Assertion Based On ExperimentIDA:UniProtKB
MitophagyManual Assertion Based On ExperimentIDA:UniProtKB

Cytoplasmic vesicle, autophagosome membrane
Endomembrane system
Mitochondrion membrane
Cytoplasm, cytoskeleton
Cytoplasmic vesicle
LC3-II binds to the autophagic membranes. LC3-II localizes with the mitochondrial inner membrane during Parkin-mediated mitophagy (PubMed:28017329).
Localizes also to discrete punctae along the ciliary axoneme

The precursor molecule is cleaved by ATG4 (ATG4A, ATG4B, ATG4C or ATG4D) to expose the glycine at the C-terminus and form the cytosolic form, LC3-I (PubMed:15187094, PubMed:15355958, PubMed:20818167, PubMed:29458288, PubMed:30661429, PubMed:31315929).
The processed form is then activated by APG7L/ATG7, transferred to ATG3 and conjugated to phosphatidylethanolamine (PE) phospholipid to form the membrane-bound form, LC3-II (PubMed:15187094).
During non-canonical autophagy, the processed form is conjugated to phosphatidylserine (PS) phospholipid (PubMed:33909989).
ATG4 proteins also mediate the delipidation of PE-conjugated forms (PubMed:29458288, PubMed:33909989).
In addition, ATG4B and ATG4D mediate delipidation of ATG8 proteins conjugated to PS during non-canonical autophagy (PubMed:33909989).
ATG4B constitutes the major protein for proteolytic activation (PubMed:30661429).
ATG4D is the main enzyme for delipidation activity (By similarity).
(Microbial infection) The Legionella effector RavZ is a deconjugating enzyme that hydrolyzes the amide bond between the C-terminal glycine residue and an adjacent aromatic residue in ATG8 proteins conjugated to phosphatidylethanolamine (PE), producing an ATG8 protein that is resistant to reconjugation by the host machinery due to the cleavage of the reactive C-terminal glycine (PubMed:23112293, PubMed:28395732, PubMed:31722778).
RavZ is also able to mediate delipidation of ATG8 proteins conjugated to phosphatidylserine (PS) (PubMed:33909989).
Phosphorylation by PKA inhibits conjugation of phosphatidylethanolamine (PE) (PubMed:22948227).
Interaction with MAPK15 reduces the inhibitory phosphorylation and increases autophagy activity (PubMed:22948227).