TMEM59

Also known as C1orf8, HSPC001, DCF1, PRO195, UNQ169, transmembrane protein 59

Transmembrane protein 59 is a protein that in humans is encoded by the TMEM59 gene.

Gene data

TMEM59

Name: transmembrane protein 59
Type: protein-coding
Position: 54,026,681–54,053,504 (−)
Aliases: C1orf8, DCF1, HSPC001, PRO195, UNQ169
Ensembl: ENSG00000116209
RefSeq RNA: NM_001305043.2, NM_001305049.1, NM_001305050.2, NM_001305051.1, NM_001305052.1
RefSeq protein: NP_001291972.1, NP_001291978.1, NP_001291979.1, NP_001291980.1, NP_001291981.1

This gene encodes a protein shown to regulate autophagy in response to bacterial infection. This protein may also regulate the retention of amyloid precursor protein (APP) in the Golgi apparatus through its control of APP glycosylation. Overexpression of this protein has been found to promote apoptosis in a glioma cell line. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Feb 2015].

Gene Ontology

Biological process

glycoprotein biosynthetic process positive regulation of autophagy positive regulation of autophagy negative regulation of protein localization to plasma membrane

Molecular function

endopeptidase activity protein binding

Cellular component

Golgi cis cisterna Golgi trans cisterna Golgi membrane lysosome lysosome lysosomal membrane late endosome late endosome

Pathways

Signal Transduction Signaling by Rho GTPases RHO GTPase cycle RHOH GTPase cycle RND1 GTPase cycle Signaling by Rho GTPases, Miro GTPases and RHOBTB3

via MyGene.info

Wikidata facts

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HomoloGene ID: 3583
exact match: identifiers.org/ncbigene/9528
genomic end: 54519177
genomic start: 54497347
cytogenetic location: 1p32.3

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Transmembrane protein 59 is a protein that in humans is encoded by the TMEM59 gene.

TMEM59 is a membrane bound protein that is localized to the Golgi apparatus. The precise function of TMEM59 is not known, however it has been demonstrated that expression of TMEM59 protein inhibits Golgi glycosylation of amyloid precursor protein (APP) and blocks APP cleavage by the α- and β-amyloid precursor protein secretases and therefore inhibits formation of the beta amyloid peptide that forms amyloid plaques in Alzheimer's disease. Moreover, TMEM59 has been shown to potentiate wnt signaling by promoting formation of the wnt receptor signalosomes. Transmembrane interactions between TMEM59 and the wnt receptor Frizzled were found to drive receptor multimerization that leads to improved potency and efficacy of wnt signaling.