AFfirm™ TEX264 Mouse Monoclonal Antibody - #BF8813

Major reticulophagy (also called ER-phagy) receptor that acts independently of other candidate reticulophagy receptors to remodel subdomains of the endoplasmic reticulum into autophagosomes upon nutrient stress, which then fuse with lysosomes for endoplasmic reticulum turnover. The ATG8-containing isolation membrane (IM) cradles a tubular segment of TEX264-positive ER near a three-way junction, allowing the formation of a synapse of 2 juxtaposed membranes with trans interaction between the TEX264 and ATG8 proteins. Expansion of the IM would extend the capture of ER, possibly through a 'zipper-like' process involving continued trans TEX264-ATG8 interactions, until poorly understood mechanisms lead to the fission of relevant membranes and, ultimately, autophagosomal membrane closure.

Endoplasmic reticulum membrane>Single-pass type III membrane protein. Cytoplasmic vesicle>Autophagosome.
Note: Is trafficked from tubular ER to growing autophagosomes via its cytosolic LIR motif.

Interacts (via the LIR motif) with ATG8 family proteins MAP1LC3A, MAP1LC3B, GABARAP and GABARAPL1.

The LIR motif in the cytosol-facing C-terminal region is involved in the interaction with ATG8 proteins.

The long intrinsically disordered region (IDR) is required for autophagosome binding and reticulophagy, probably via bridging the long distance between endoplasmic reticulum and autophagosome membranes, because ribosomes exist on endoplasmic reticulum membranes that attach to autophagic membranes.