ArticleCommunications biology2023
Transmembrane protein 135 regulates lipid homeostasis through its role in peroxisomal DHA metabolism.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- TMEM135 deficiency prevents intestinal lipid accumulation by coordinating lipid uptake and oxidation through ELOVL6-mediated PPARα activation.Experimental & molecular medicine · 2026Article
- Transmembrane protein TMEM98 as a multifunctional regulator in cancer: from signaling pathways to translational implications.Journal of translational medicine · 2025Review
- Unveiling the reproductive risks of PFOS: testicular proteome disruption and hormonal imbalance in male rats†.Biology of reproduction · 2025Article
- A mutation in Tmem135 causes progressive sensorineural hearing loss.Hearing research · 2025Article
- Association Between C22:5-Containing Lipids and RPE Pathologies in Mice with Tmem135 Overexpression.Advances in experimental medicine and biology · 2025Article
- Traumatic brain injury reprograms lipid droplet metabolism shaped by aging and diet in Drosophila brain.PloS one · 2025Article
- Hepatic Transcriptomics of Broilers with Low and High Feed Conversion in Response to Caloric Restriction.Metabolites · 2024Article
- Acyl-CoA synthetase 6 controls rod photoreceptor function and survival by shaping the phospholipid composition of retinal membranes.Communications biology · 2024Article
- The peroxisome: an update on mysteries 3.0.Histochemistry and cell biology · 2024Review
- Roles of transmembrane protein 135 in mitochondrial and peroxisomal functions - implications for age-related retinal disease.Frontiers in ophthalmology · 2024Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
Transmembrane protein 135 (TMEM135) is thought to participate in the cellular response to increased intracellular lipids yet no defined molecular function for TMEM135 in lipid metabolism has been identified. In this study, we performed a lipid analysis of tissues from Tmem135 mutant mice and found striking reductions of docosahexaenoic acid (DHA) across all Tmem135 mutant tissues, indicating a role of TMEM135 in the production of DHA. Since all enzymes required for DHA synthesis remain intact in Tmem135 mutant mice, we hypothesized that TMEM135 is involved in the export of DHA from peroxisomes. The Tmem135 mutation likely leads to the retention of DHA in peroxisomes, causing DHA to be degraded within peroxisomes by their beta-oxidation machinery. This may lead to generation or alteration of ligands required for the activation of peroxisome proliferator-activated receptor a (PPARa) signaling, which in turn could result in increased peroxisomal number and beta-oxidation enzymes observed in Tmem135 mutant mice. We confirmed this effect of PPARa signaling by detecting decreased peroxisomes and their proteins upon genetic ablation of Ppara in Tmem135 mutant mice. Using Tmem135 mutant mice, we also validated the protective effect of increased peroxisomes and peroxisomal beta-oxidation on the metabolic disease phenotypes of leptin mutant mice which has been observed in previous studies. Thus, we conclude that TMEM135 has a role in lipid homeostasis through its function in peroxisomes.
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