Ask about this productRelated genes to: SAMM50 antibody
- Gene:
- SAMM50 NIH gene
- Name:
- SAMM50 sorting and assembly machinery component
- Previous symbol:
- -
- Synonyms:
- CGI-51, TRG-3, YNL026W, OMP85, TOB55, SAM50
- Chromosome:
- 22q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2005-05-31
- Date modifiied:
- 2016-07-04
Related products to: SAMM50 antibody
Related articles to: SAMM50 antibody
- Although Sorting and Assembly Machinery 50 (SAM50) is known to regulate nutritional and metabolic stress related to ageing, its exact role is not well understood. This experimental study combines both human and animal models to understand the role that SAM50 plays in nutrient, age-related metabolic remodeling. We also wanted to define the clinical relevance of SAMM50 genetic variation in human disease. Our study integrated clinical and genetic data from three large and independent human biobanks to assess the clinical implications of genetic variation in SAMM50. We then conducted mechanistic studies in mice using Serial Block-Face Scanning Electron Microscopy and Transmission Electron Microscopy for three-dimension analysis of mitochondrial morphology, immunoblotting, metabolomics/lipidomics, and assessment of metabolic parameters in models of fasting, aging, and a high-fat diet (HFD). Descriptive and inferential statistics were used to describe and test associations in GraphPad prism version 10. Our study demonstrated that common genetic variation within the SAMM50 genetic locus was significantly associated with liver-related metabolic disorders. In mice, nutrient status was associated with expression levels of Sam50 and proteins involved in the respiratory complex. Aging was associated with impaired mitochondria, decreased Sam50 expression, and increased triglyceride and lipid peroxidation, with increased lipid droplet-mitochondria contacts. An HFD was associated with a reduction in Sam50 expression, disruption of mitochondrial structure, and metabolic dysfunction, effects that were only partly reversed by returning to a normal diet. Our results demonstrate that SAM50 expression is associated with nutrient state and age-related signals, thereby orchestrating mitochondrial structure to influence systemic metabolic health. - Source: PubMed
Publication date: 2026/02/16
Hinton Antentor OthrellMasenga Sepiso KBaskerville VictoriaPetrovic MarkRodriguez BenjaminHubert David LMiller-Fleming Tyne WKoo Young DoKatti PrasannaVenkhatesh PrasannaKirabo AnnetLopez Edgar GarzaCrabtree AmberMarshall AndreaBlake CampbellDash ChandravanuPrasad PraveenaMurphy AlexandriaAfolabi JeremiahPhillips Mark AEvans ChantellScudese EstevãoSchafer Jenny CBerry JuliaMobley Bret CDai Dao FuMobley HarrisonWinn Nathan CKhan Mohd MPulatani DeaSorrentino JosephGamble-George JoyonnaMcReynolds MelanieWanjalla Celestine - Sarcopenia, characterized by age-related skeletal muscle loss and dysfunction, affects approximately 10% of adults over 60 years worldwide. Current diagnostic methods often detect sarcopenia only after substantial muscle deterioration has occurred, highlighting the critical need for early diagnostic biomarkers. - Source: PubMed
Publication date: 2026/02/09
Ying HonganWang WenhanHuang LiliHong WeiwenYang Lingchang - Diabetic foot ulcer (DFU) is one of the most common and severe complications of diabetes, with vascular changes, neuropathy, and infections being the primary pathological mechanisms. Disulfidptosis, a recently identified form of programmed cell death, might be involved in the development of diabetic complications. This study aims to identify and validate potential disulfidptosis biomarkers associated with DFU through bioinformatics and machine learning analysis. - Source: PubMed
Publication date: 2025/10/08
Li JIeShi HongshuoCao Yemin - Few genome-wide association studies have examined genetic variants associated with hepatocellular carcinoma (HCC) risk in individuals seronegative for HBsAg and anti-HCV, and the long-term impact of these variants remains uncertain. - Source: PubMed
Publication date: 2025/11/11
Liu Xia-RongYang Tsai-HsuanSu Tung-HungYin Szu-ChingChen Yi-TingChen Fen-FangPang See-TongHou Ming-ChihPeng Yen-ChunYang Shun-FaHuang Peng-JuLee Sing-LianChen MingHuang Chih-YangChang Ya-HsuanChen Hsuan-YuYang Hwai-IYu Ming-LungChen Chien-JenKao Jia-HorngLee Mei-Hsuan - Nuclear androgen receptor (AR) dysregulation characterizes polycystic ovary syndrome (PCOS) pathophysiology and contributes to mitochondrial dysfunction-related adverse pregnancy outcomes. However, ARs also localize to mitochondria in many cell types, and mitochondrial dysfunction is implicated in the underlying pathogenesis of PCOS. In this study, human endometrial decidual basalis tissues and rat gravid uterine tissues were collected, and subcellular fractionation, western blot, quantitative real-time polymerase chain reaction (qPCR), electron microscopy, and enzyme-linked immunosorbent assay (ELISA) were conducted. PCOS patients with early pregnancy exhibited increased expression of AR mRNA and mitochondrial AR protein in decidual basalis. Similar alterations of AR levels were also observed in gravid uterus of 5α-dihydrotestosterone (DHT) + insulin-exposed pregnant rats with fetal loss. In both PCOS patients and DHT + insulin-exposed pregnant rats, uterine mitochondria displayed disorganized cristae along with decreased uterine mitochondrial DNA (mtDNA) content and reduced expression of mitochondrial morphogenesis (mito-morphosis) genes (sorting and assembly machinery component 50 (SAMM50), coiled-coil helix coiled-coil helix domain-containing protein 3 (CHCHD3), and dynamin-related protein 1 (DRP1)) and total adenosine triphosphate (ATP) levels. In addition, there was dysregulated expression of mitochondrial fusion and fission, biogenesis, mitophagy, and mitochondrial ribosome protein gene. In DHT + insulin-exposed pregnant rats, treatment with flutamide prevented fetal loss and partially rescued mitochondrial morphological abnormalities in uterine decidual stromal cells. In addition, flutamide normalized uterine Ar mRNA and mitochondrial AR protein expression; inner membrane mitochondrial protein (Immt), ras homolog enriched in brain protein (Rheb), and Mrp7 mRNA expression; and the Parkin:PTEM-induced putative kinase 1 (Pink1) ratio and restored total nicotinamide adenine dinucleotide (NAD) and ATP contents. Collectively, this work identifies mitochondrial AR in the uterus and implicates hyperandrogenism-induced, AR-dependent mitochondrial dysfunction in decidual stromal cells as a key mechanism underlying pregnancy loss in PCOS. - Source: PubMed
Publication date: 2026/01/28
Zhang YuehuiHu MinShao Linus RLu LingjingHan JingGuo TingtingJiang MengWu YaoHan HanCui PengBrännström MatsSferruzzi-Perri Amanda NancyBillig Håkan