ArticleTraffic (Copenhagen, Denmark)2014
Cellular zinc levels are modulated by TRPML1-TMEM163 interaction.
Article in Traffic (Copenhagen, Denmark), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
41 citing papers in PubMed, 59 citations in OpenAlex.
- A dileucine motif in TMEM163 is essential for its binding with both AP-3 and BLOC-1 complex.The Journal of biological chemistry · 2026Article
- A Genome-wide Association Study of Alzheimer's Disease and Dementia in a Large Multi-ancestry Military Cohort Identifies Many New Dementia-Associated Loci.medRxiv : the preprint server for health sciences · 2026Article
- Lysosomal zinc nanomodulation blocks macrophage pyroptosis for counteracting atherosclerosis progression.Science advances · 2025Article
- The role of TMEM163 protein in thyroid microcarcinoma: expression pattern and clinical implications.Journal of endocrinological investigation · 2025Article
- Genomic insights into runs of homozygosity, effective population size and selection signatures in Iranian meat and dairy sheep breeds.PloS one · 2025Article
- The role of Zn2+ in shaping intracellular Ca2+ dynamics in the heart.The Journal of general physiology · 2023Review
- Selective dopaminergic vulnerability in Parkinson's disease: new insights into the role of DAT.Frontiers in neuroscience · 2023Review
- Expanding the Toolbox: Novel Modulators of Endolysosomal Cation Channels.Handbook of experimental pharmacology · 2023Article
- Variants in the zinc transporter TMEM163 cause a hypomyelinating leukodystrophy.Brain : a journal of neurology · 2022Article
- Transmembrane 163 (TMEM163) protein interacts with specific mammalian SLC30 zinc efflux transporter family members.Biochemistry and biophysics reports · 2022Article
- Functional Study ofCells · 2022Article
- Article
- The intracellular cation channel TMEM176B as a dual immunoregulator.Frontiers in cell and developmental biology · 2022Review
- Genetic Analysis of Six Transmembrane Protein Family Genes in Parkinson's Disease in a Large Chinese Cohort.Frontiers in aging neuroscience · 2022Article
- Lysosomal ZnCell reports · 2021Article
- Genetic Associations with Weight Gain among South Africans who Initiated Dolutegravir-Containing and Tenofovir-Containing Regimens.Journal of acquired immune deficiency syndromes (1999) · 2021Article
- A zinc transporter, transmembrane protein 163, is critical for the biogenesis of platelet dense granules.Blood · 2021Article
- Zinc: Multidimensional Effects on Living Organisms.Biomedicines · 2021Review
- Transmembrane 163 (TMEM163) Protein: A New Member of the Zinc Efflux Transporter Family.Biomedicines · 2021Review
- Protocol for Quantifying Zinc Flux in Cultured Cells using Fluorescent Indicators.STAR protocols · 2020Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Mucolipidosis type IV (MLIV) is caused by loss of function mutations in the TRPML1 ion channel. We previously reported that tissue zinc levels in MLIV were abnormally elevated; however, the mechanism behind this pathologic accumulation remains unknown. Here, we identify transmembrane (TMEM)-163 protein, a putative zinc transporter, as a novel interacting partner for TRPML1. Evidence from yeast two-hybrid, tissue expression pattern, co-immunoprecipitation, mass spectrometry and confocal microscopy studies confirmed the physical association of TMEM163 with TRPML1. This interaction is disrupted when a part of TMEM163's N-terminus was deleted. Further studies to define the relevance of their interaction revealed that the plasma membrane (PM) levels of TMEM163 significantly decrease when TRPML1 is co-expressed in HEK-293 cells, while it mostly localizes within the PM when co-expressed with a mutant TRPML1 that distributes mostly in the PM. Meanwhile, co-expression of TMEM163 does not alter TRPML1 channel activity, but its expression levels in MLIV patient fibroblasts are reduced, which correlate with marked accumulation of zinc in lysosomes when these cells are acutely exposed to exogenous zinc (100 μM). When TMEM163 is knocked down or when TMEM163 and TRPML1 are co-knocked down in HEK-293 cells treated overnight with 100 nm zinc, the cells have significantly higher intracellular zinc levels than untreated control. Overall, these findings suggest that TMEM163 and TRPML1 proteins play a critical role in cellular zinc homeostasis, and thus possibly explain a novel mechanism for the pathological overload of zinc in MLIV disease.
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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.