ArticleBrain : a journal of neurology2020
A role of the frontotemporal lobar degeneration risk factor TMEM106B in myelination.
Article in Brain : a journal of neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 50 citations in OpenAlex.
- Article
- Beyond Neurodegeneration: White Matter Vacuolation as a Primary Myelin Defect.International journal of molecular sciences · 2026Review
- TMEM106B C-terminal fragments drive nucleocytoplasmic transport failure and TDP-43 mislocalization in the aging human brain.bioRxiv : the preprint server for biology · 2026Article
- The amyloidogenic C-terminal region of TMEM106B modulates lipid membrane biophysical properties: Functional and pathological insights.The Journal of biological chemistry · 2026Article
- Real-time pH imaging of macrophage lysosomes using the pH-sensitive probe ApHID.Cell reports methods · 2025Article
- NAT10 Increases Lysosomal Acidification to Promote Esophageal Cancer Metastasis via ac4C Acetylation of ATP6V0E1 mRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The role of endolysosomal progranulin and TMEM106B in neurodegenerative diseases.Molecular neurodegeneration · 2025Review
- TMEM106B Supports Viral Entry and Syncytia Formation Mediated by the Spike Proteins From Omicron BA.2.86 and JN.1.Journal of medical virology · 2025Article
- LncRNA-induced lysosomal localization of NHE1 promotes increased lysosomal pH in macrophages leading to atherosclerosis.The Journal of biological chemistry · 2025Article
- Defining diverse spike-receptor interactions involved in SARS-CoV-2 entry: Mechanisms and therapeutic opportunities.Virology · 2025Review
- Increased TMEM106B levels lead to lysosomal dysfunction which affects synaptic signaling and neuronal health.Molecular neurodegeneration · 2025Article
- Progranulin deficiency in the brain: the interplay between neuronal and non-neuronal cells.Translational neurodegeneration · 2025Review
- TMEM106B deficiency leads to alterations in lipid metabolism and obesity in the TDP-43Communications biology · 2025Article
- TMEM106B Knockdown Exhibits a Neuroprotective Effect in Parkinson's Disease via Decreasing Inflammation and Iron Deposition.Molecular neurobiology · 2025Article
- White matter pathology in FTLD caused by GRN mutations.Acta neuropathologica · 2025Article
- Lysosomal TMEM106B interacts with galactosylceramidase to regulate myelin lipid metabolism.Communications biology · 2024Article
- Hypomyelination Leukodystrophy 16 (HLD16)-Associated Mutation p.Asp252Asn of TMEM106B Blunts Cell Morphological Differentiation.Current issues in molecular biology · 2024Article
- Physiological and pathological functions of TMEM106B in neurodegenerative diseases.Cellular and molecular life sciences : CMLS · 2024Review
- Loss of TMEM106B exacerbates Tau pathology and neurodegeneration in PS19 mice.Acta neuropathologica · 2024Article
- Loss of TMEM106B exacerbates Tau pathology and neurodegeneration in PS19 mice.bioRxiv : the preprint server for biology · 2023Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
TMEM106B encodes a lysosomal membrane protein and was initially identified as a risk factor for frontotemporal lobar degeneration. Recently, a dominant D252N mutation in TMEM106B was shown to cause hypomyelinating leukodystrophy. However, how TMEM106B regulates myelination is still unclear. Here we show that TMEM106B is expressed and localized to the lysosome compartment in oligodendrocytes. TMEM106B deficiency in mice results in myelination defects with a significant reduction of protein levels of proteolipid protein (PLP) and myelin oligodendrocyte glycoprotein (MOG), the membrane proteins found in the myelin sheath. The levels of many lysosome proteins are significantly decreased in the TMEM106B-deficient Oli-neu oligodendroglial precursor cell line. TMEM106B physically interacts with the lysosomal protease cathepsin D and is required to maintain proper cathepsin D levels in oligodendrocytes. Furthermore, we found that TMEM106B deficiency results in lysosome clustering in the perinuclear region and a decrease in lysosome exocytosis and cell surface PLP levels. Moreover, we found that the D252N mutation abolished lysosome enlargement and lysosome acidification induced by wild-type TMEM106B overexpression. Instead, it stimulates lysosome clustering near the nucleus as seen in TMEM106B-deficient cells. Our results support that TMEM106B regulates myelination through modulation of lysosome function in oligodendrocytes.
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