TMEM59

TMEM59 is a protein shown to regulate autophagy in response to bacterial infection. TMEM59 may also regulate the retention of amyloid precursor protein (APP) in the Golgi apparatus through its control of APP glycosylation. Overexpression of TMEM59 has been found to promote apoptosis in a glioma cell line.

Transmembrane Protein 59

Acts as a regulator of autophagy in response to S.aureus infection by promoting activation of LC3 (MAP1LC3A, MAP1LC3B or MAP1LC3C). Acts by interacting with ATG16L1, leading to promote a functional complex between LC3 and ATG16L1 and promoting LC3 lipidation and subsequent activation of autophagy (PubMed:27273576, PubMed:23376921).
Modulates the O-glycosylation and complex N-glycosylation steps occurring during the Golgi maturation of several proteins such as APP, BACE1, SEAP or PRNP (PubMed:20427278).
Inhibits APP transport to the cell surface and further shedding (PubMed:20427278).

Biological Process autophagySource:UniProtKB-KW
Biological Process negative regulation of protein localization to plasma membraneSource:UniProtKB1 Publication
Biological Process positive regulation of autophagySource:UniProtKB1 Publication
Biological Process protein glycosylationSource:UniProtKB1 Publication

Late endosome membrane
Lysosome membrane
Cell membrane
Golgi apparatus membrane
Mainly localizes to late endosomes/lysosomes. Probably first exported to the cell surface and then actively endocytosed to transiently localize in early endosomes on its way to the late endosomal/lysosomal compartment where it becomes quickly degraded.

Extracellular: 36-238
Helical: 239-259
Cytoplasmic: 260-323

N-glycosylated.