Ask about this productRelated genes to: TMEM135 antibody
- Gene:
- TMEM135 NIH gene
- Name:
- transmembrane protein 135
- Previous symbol:
- -
- Synonyms:
- FLJ22104
- Chromosome:
- 11q14.2
- Locus Type:
- gene with protein product
- Date approved:
- 2006-03-09
- Date modifiied:
- 2019-03-20
Related products to: TMEM135 antibody
Related articles to: TMEM135 antibody
- Osteoporosis and fractures are major health concerns. We developed and validated a polygenic score (PGS) for quantitative ultrasound (QUS)-defined osteoporosis risk in Japanese individuals using heel QUS-derived T-scores. Genome-wide association study summary statistics from up to 10,794 participants in the Tohoku Medical Megabank Community-Based Cohort identified genome-wide significant loci, including MBL2, TMEM135, and WNT16. PGS models were constructed and evaluated using independent datasets for model selection (n = 1419) and validation (n = 8711). Adding the PGS to age and sex yielded only modest improvements in discrimination, whereas PGS quintiles supported genetic risk stratification. Compared with the intermediate group, individuals in the lowest PGS quintile had higher odds of the outcome (1.22, 95% confidence interval [CI]: 1.07-1.40), whereas those in the highest quintile had lower odds (0.85, 95% CI: 0.74-0.98). During prospective follow-up (mean 3.5 years), a similar gradient was observed, with higher incidence rate ratios in the lowest quintile (1.42, 95% CI: 1.17-1.73) and lower incidence rate ratios in the highest quintile (0.70, 95% CI: 0.54-0.89). No statistically significant interaction between age and PGS was observed, and age-T-score regression analyses showed no differences in age-related T-score decline across genetic risk groups. However, analyses in young adults (20-44 years) and extrapolation to age 20 suggested lower bone status around peak bone mass in individuals at high genetic risk for QUS-defined osteoporosis. These findings suggest that a Japanese-specific PGS may help identify individuals at elevated genetic risk earlier in adulthood. - Source: PubMed
Publication date: 2026/09/09
Otsuka-Yamasaki YayoiSutoh YoichiHachiya TsuyoshiNakao MotokiMinabe ShioriKomaki ShoheiOhmomo HidekiSasaki MakotoShimizu Atsushi - Excessive lipid accumulation impairs digestion and gastrointestinal function. Transmembrane protein 135 (TMEM135) is involved in lipid metabolism of various tissues. Here, TMEM135 deficiency increased intestinal lipid absorption through ELOVL6-dependent oleoylethanolamide production and subsequent activation of peroxisome proliferator-activated receptor alpha (PPARα), which upregulated CD36 at the plasma membrane in the intestine of mice fed a high-fat diet or lard oil. Despite this enhanced lipid uptake, long-term lipid accumulation was suppressed by elevated peroxisomal and mitochondrial β-oxidation through increased fatty acid oxidation and oxidative phosphorylation activities without chylomicron secretion in TMEM135-depleted intestine. Inhibition of PPARα or ELOVL6 attenuated these effects. Furthermore, consistent results were observed in both TMEM135 KO and intestine-specific TMEM135 mice, confirming tissue-specific rather than systemic effects. Overall, these results provide insight into the role of TMEM135 as a regulatory node connecting intestinal lipid absorption and systemic energy expenditure, contributing to the coordination between lipid storage and oxidation during metabolic adaptation. - Source: PubMed
Publication date: 2026/08/05
Kim HyunsooPark ChannyWei XiaofanChhetri ArunManandhar LaxmanSeo JiwonPark YoonkyungLee Sang-WookPark Raekil - TMEM135 has been implicated in lipid metabolism, but its role in regulating hepatic lipid homeostasis remains unclear. Here, we investigated how TMEM135 affects hepatic lipid metabolism using mutant mice with liver-specific deletion. The mutation induced a lipogenic state characterized by depletion of docosahexaenoic acid (DHA), activation of SREBP-dependent pathways, and increased monounsaturated fatty acids without causing hepatic steatosis. In contrast, loss of PEX5-dependent peroxisomal function in mutant mice resulted in marked hepatic lipid accumulation, indicating that peroxisomal metabolism buffers the elevated lipogenic state. Fish oil supplementation to mutant mice restored DHA levels and suppressed lipogenesis. Proteomics identified distinct DHA-sensitive metabolic programs, including activation of SREBP-dependent lipogenesis. Quantitative malonyl-proteomics revealed increased malonylation of glycolytic enzymes, accompanied by altered glycolytic output. Together, these findings identify TMEM135 as a central regulator of hepatic lipid metabolism and uncover a coordinated mechanism linking lipid availability, lipogenesis, and post-translational metabolic regulation. - Source: PubMed
Publication date: 2026/07/23
Hagimori RyoLandowski MichaelSong SiyuGogoi PurnimaBrush Richard SBonvicino Sarah MBarrett-Wilt GregIkeda SakaeYamada Ken-IchiYen Chi-Liang EricTakimoto TetsuyaAgbaga Martin-PaulIkeda Akihiro - Transmembrane protein 135 (TMEM135) is a highly conserved 52 kDa protein with five predicted transmembrane domains that colocalizes with mitochondria and peroxisomes. Previous studies have shown that TMEM135 is involved in mitochondrial dynamics, thermogenesis, and lipid metabolism across multiple tissues and species; however, its role in the inner ear and auditory system remains unknown. We investigated the function of TMEM135 in hearing using wild-type (WT) and Tmem135 (FUN025) mutant mice on a CBA/CaJ background, a normal-hearing mouse strain. Although FUN025 mice displayed normal auditory brainstem response (ABR) thresholds at 1 month, we observed significantly elevated ABR thresholds at 8, 16, and 64 kHz by 3 months, which progressed to profound hearing loss by 12 months. Consistent with our auditory testing results, 13-month-old FUN025 mice exhibited a severe loss of outer hair cells and more modest changes in inner hair cell survival, spiral ganglion neuron density, and stria vascularis integrity in the cochlea. Our results using BaseScope RNA in situ hybridization indicate that TMEM135 is expressed in the inner hair cells, outer hair cells, supporting cells, and stria vascularis. Using Volocity software and Costes colocalization analysis, we found that TMEM135 closely colocalizes with mitochondria in hair cells. Together, these results demonstrate that the FUN025 mutation in Tmem135 causes progressive sensorineural hearing loss, and suggest that TMEM135 is crucial for maintaining key cochlear cell types and normal sensory function in the aging cochlea. - Source: PubMed
Publication date: 2025/02/14
Kim Mi-JungSimms ShionBehnammanesh GhazalehChen Wei-WenHonkura YoheiSuzuki JunPark Hyo-JinMilani MarcusKatori YukioBird Jonathan EIkeda AkihiroSomeya Shinichi - Dysregulation of lipid metabolism has been linked with risk for age-related retinal diseases including age-related macular degeneration (AMD). However, how dysregulated lipid metabolism contributes to AMD development is unknown. In this study, we evaluated the retinal and plasma lipidomes of a mouse model displaying retinal pigmented epithelium (RPE) pathologies that are observed in AMD including RPE dysmorphia and degeneration. We found that the RPE phenotypes in mice overexpressing transmembrane protein 135 (Tmem135 TG) are correlated with retinal and plasma lipidome changes. While distinct lipid profiles were observed in the retina and plasma of Tmem135 TG mice, a common finding in both retinal and plasma lipidomes was an increase of lipids containing C22:5. This data suggests that accumulation of C22:5-containing lipids may contribute to the development of the RPE pathologies in Tmem135 TG mice. - Source: PubMed
Landowski MichaelIkeda SakaeIkeda Akihiro