ArticleCell death & disease2020
TMEM59 interacts with TREM2 and modulates TREM2-dependent microglial activities.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- TMEM59 regulates microglial Aβ phagocytosis in a TREM2-dependent manner and acts as a potential therapeutic target for Aβ amyloidosis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Mll5 haploinsufficiency attenuates microglial phagocytosis through dysregulated TREM2-SGK3-GSK3β signaling and recapitulates ASD-like behaviors in mice.Nature communications · 2026Article
- Intervention of ginseng-derived macromolecular drugs in Alzheimer's disease: exploring mechanisms and assessing potential.Frontiers in aging neuroscience · 2026Review
- TREM2 as a central hub of neuroimmune-metabolic crosstalk in central nervous system disorders: from microglial biology to therapeutic targeting.Frontiers in immunology · 2026Review
- Glycosylation in neuroinflammation: mechanisms, implications, and therapeutic strategies for neurodegenerative diseases.Translational neurodegeneration · 2025Review
- Review
- TMEM59 deficiency activates chaperone-mediated autophagy and ameliorates disease-like pathologies in tauopathy model mice.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- TREM 2 in Parkinson's Disease: A Promising Candidate Gene for Disease Susceptibility and Progression.Brain sciences · 2025Review
- Influence of CCancers · 2023Article
- Molecular Regulation Mechanism of Microglial Autophagy in the Pathology of Alzheimer's Disease.Aging and disease · 2023Review
- Blood leukocyte transcriptional modules and differentially expressed genes associated with disease severity and age in COVID-19 patients.Scientific reports · 2023Article
- Regulated necrosis pathways: a potential target for ischemic stroke.Burns & trauma · 2023Review
- An Analysis of the Gene Expression Associated with Lymph Node Metastasis in Colorectal Cancer.International journal of genomics · 2023Article
- MicroglialThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- A transmembrane protein family gene signature for overall survival prediction in osteosarcoma.Frontiers in genetics · 2022Article
- Genetic Analysis of Six Transmembrane Protein Family Genes in Parkinson's Disease in a Large Chinese Cohort.Frontiers in aging neuroscience · 2022Article
- Transcriptome and Translatome Regulation of Pathogenesis in Alzheimer's Disease Model Mice.Journal of Alzheimer's disease : JAD · 2022Article
- TREM-2 is a sensor and activator of T cell response in SARS-CoV-2 infection.Science advances · 2021Article
- Autophagy & Phagocytosis in Neurological Disorders and their Possible Cross-talk.Current neuropharmacology · 2021Review
- Psychological Stress as a Risk Factor for Accelerated Cellular Aging and Cognitive Decline: The Involvement of Microglia-Neuron Crosstalk.Frontiers in molecular neuroscience · 2021Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The surface receptor triggering receptor expressed on myeloid cells 2 (TREM2) plays a crucial role in maintaining a multitude of microglial activities, such as survival, proliferation, migration, metabolism, inflammation, and phagocytosis. However, the molecular mechanisms underlying TREM2-mediated microglial activities remain largely elusive. Herein, we found that TREM2 interacted with the type I transmembrane protein TMEM59, whose expression could facilitate autophagic flux through its carboxyl-terminus. TMEM59 expression was decreased upon lipopolysaccharide treatment. While downregulation of TMEM59 promoted anti-inflammatory factor expression and attenuated lipopolysaccharide treatment-induced inflammation. Importantly, we found that overexpression of TREM2 reduced TMEM59 protein levels through promoting its degradation, whereas TMEM59 levels were elevated in Trem2-deficient microglia. Finally, impaired survival, proliferation, migration, and phagocytosis, as well as dysregulated autophagy and metabolism in Trem2-deficient microglia were attenuated upon TMEM59 silencing. Together, our findings reveal a novel function of TREM2 in mediating TMEM59 protein degradation and demonstrate the importance of TMEM59 homeostasis in maintaining TREM2-mediated microglial activities.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.