ArticleThe Journal of biological chemistry2010
The novel membrane protein TMEM59 modulates complex glycosylation, cell surface expression, and secretion of the amyloid precursor protein.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 71 citations in OpenAlex.
- TMEM59L promotes neuroendocrine differentiation and enzalutamide resistance in prostate cancer by regulating MUC1/β-catenin/MYC axis.Clinical and translational medicine · 2026Article
- Unique Expression and Glycosylation of Amyloid Precursor Protein in Alzheimer's Disease.Advances in experimental medicine and biology · 2026Review
- Single-Cell Analysis Combined with Mendelian Randomization Identifies Genes Associated with Prostate Cancer Cells.The world journal of men's health · 2026Article
- Glycosylation in neuroinflammation: mechanisms, implications, and therapeutic strategies for neurodegenerative diseases.Translational neurodegeneration · 2025Review
- Single-cell and clonal analysis of AL amyloidosis plasma cells and their bone marrow microenvironment.Blood · 2025Article
- DNA Methylation in Alzheimer's Disease.Current topics in behavioral neurosciences · 2025Review
- The Landscape of m6A Regulators in Multiple Brain Regions of Alzheimer's Disease.Molecular neurobiology · 2023Article
- Prognostic value of TMEM59L and its genomic and immunological characteristics in cancer.Frontiers in immunology · 2022Article
- Transcriptome and Translatome Regulation of Pathogenesis in Alzheimer's Disease Model Mice.Journal of Alzheimer's disease : JAD · 2022Article
- The role of the integral type II transmembrane protein BRI2 in health and disease.Cellular and molecular life sciences : CMLS · 2021Review
- Investigation of LINC00493/SMIM26 Gene Suggests Its Dual Functioning at mRNA and Protein Level.International journal of molecular sciences · 2021Article
- Whole exome sequencing, in silico and functional studies confirm the association of theSaudi journal of biological sciences · 2021Article
- What Can N-glycomics and N-glycoproteomics of Cerebrospinal Fluid Tell Us about Alzheimer Disease?Biomolecules · 2021Review
- Non-canonical autophagy functions of ATG16L1 in epithelial cells limit lethal infection by influenza A virus.The EMBO journal · 2021Article
- TheProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Spatial Transcriptomics Reveals Genes Associated with Dysregulated Mitochondrial Functions and Stress Signaling in Alzheimer Disease.iScience · 2020Article
- TMEM59 interacts with TREM2 and modulates TREM2-dependent microglial activities.Cell death & disease · 2020Article
- Glycan biomarkers for Alzheimer disease correlate with T-tau and P-tau in cerebrospinal fluid in subjective cognitive impairment.The FEBS journal · 2020Article
- Mutational analysis of genes with ureteric progenitor cell-specific expression in branching morphogenesis of the mouse kidney.Developmental dynamics : an official publication of the American Association of Anatomists · 2020Article
- TMEM59 Haploinsufficiency Ameliorates the Pathology and Cognitive Impairment in the 5xFAD Mouse Model of Alzheimer's Disease.Frontiers in cell and developmental biology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ectodomain shedding of the amyloid precursor protein (APP) by the two proteases alpha- and beta-secretase is a key regulatory event in the generation of the Alzheimer disease amyloid beta peptide (Abeta). At present, little is known about the cellular mechanisms that control APP shedding and Abeta generation. Here, we identified a novel protein, transmembrane protein 59 (TMEM59), as a new modulator of APP shedding. TMEM59 was found to be a ubiquitously expressed, Golgi-localized protein. TMEM59 transfection inhibited complex N- and O-glycosylation of APP in cultured cells. Additionally, TMEM59 induced APP retention in the Golgi and inhibited Abeta generation as well as APP cleavage by alpha- and beta-secretase cleavage, which occur at the plasma membrane and in the endosomes, respectively. Moreover, TMEM59 inhibited the complex N-glycosylation of the prion protein, suggesting a more general modulation of Golgi glycosylation reactions. Importantly, TMEM59 did not affect the secretion of soluble proteins or the alpha-secretase like shedding of tumor necrosis factor alpha, demonstrating that TMEM59 did not disturb the general Golgi function. The phenotype of TMEM59 transfection on APP glycosylation and shedding was similar to the one observed in cells lacking conserved oligomeric Golgi (COG) proteins COG1 and COG2. Both proteins are required for normal localization and activity of Golgi glycosylation enzymes. In summary, this study shows that TMEM59 expression modulates complex N- and O-glycosylation and suggests that TMEM59 affects APP shedding by reducing access of APP to the cellular compartments, where it is normally cleaved by alpha- and beta-secretase.
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