Ask about this productRelated genes to: MRPS15 antibody
- Gene:
- MRPS15 NIH gene
- Name:
- mitochondrial ribosomal protein S15
- Previous symbol:
- -
- Synonyms:
- FLJ11564
- Chromosome:
- 1p34.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-01-26
- Date modifiied:
- 2015-08-25
Related products to: MRPS15 antibody
Related articles to: MRPS15 antibody
- Mitochondrial homeostasis is maintained by multiple molecular chaperones and proteases located within the organelle. The mitochondrial matrix-localized protease LONP-1 degrades oxidatively damaged or misfolded proteins. Importantly, LONP-1 also regulates mitochondrial DNA replication. Here, we show that mutations in that impair LONP-1 function cause dysregulation of mitochondrial DNA replication, mitochondrial RNA transcription and protein synthesis within the mitochondrial matrix. LONP-1 deficient worms had reduced levels of oxidative phosphorylation proteins despite increased mtDNA-encoded protein synthesis. Via a forward genetic screen, we identified three mutations that restored mitochondrial function and the rate of development in mutants to levels comparable to those in wildtype worms. Interestingly, all three suppressor mutations were found in genes encoding mitochondrial ribosome proteins. A point mutation in the mitochondrial ribosome protein MRPS-38 restored oxidative phosphorylation in mutant worms. Combined, our results suggest that LONP-1 regulates mitochondrial protein synthesis and that the suppressor mutations within MRPS-38 or MRPS-15 enhance oxidative phosphorylation complex assembly by slowing translation. - Source: PubMed
Publication date: 2026/01/15
Ali LeviMallick AvijitDu YunguangLi RuiZhu Lihua JulieShen KuangHaynes Cole M - Non-obstructive azoospermia (NOA) is the severest form of male infertility. This study aimed to identify core genes associated with mitochondrial dysfunction and regulatory networks in NOA, providing potential diagnostic biomarkers and therapeutic targets for NOA. We identified mitochondrial dysfunction-related hub genes by analyzing three testis transcriptome datasets, and further confirmed their diagnostic value, differential expression in clinical specimens, and immune infiltration associations. For GSE108886 and GSE145467, 35 mitochondrial dysfunction-related differentially expressed genes (MD-DEGs, 10 upregulated and 25 downregulated) were obtained. And 6 common hub genes (COX7A1, COX7A2, COX7B2, MRPS15, AURKAIP1, and PDHA2) were identified. hsa-miR-12,116, hsa-miR-296-5p, and transcription factors (FOXA1, FOXC1, GATA2, SRF) simultaneously targeted two hub MD-DEGs. Diagnostic model incorporating COX7A1, COX7A2, AURKAIP1 and MRPS15 presented preliminary diagnostic efficacy with AUC value of 0.930 (95% CI [0.835-1.000]). Subsequently, RT-qPCR confirmed upregulation of COX7A1 (P < 0.05) and downregulation of COX7A2, COX7B2, MRPS15, AURKAIP1 and PDHA2 (P < 0.05 for all) in NOA patients. In addition, T cells CD8 and Mast cells resting were enriched in NOA patients. MD-DEGs including COX7A1, COX7A2, MRPS15 and AURKAIP1 may play pivotal roles in NOA pathogenesis, and could serve as a pre-biopsy screening tool to stratify patients and monitor therapeutic responses for NOA. - Source: PubMed
Publication date: 2026/02/04
Liu QianWu HailangYou JiaWang JingchunPeng XiangchiYe ZhenWu Menghua - This study aimed to investigate the role of poly(A) binding protein nuclear 1 (PABPN1) as a potential pan-cancer biomarker for prognosis and immunotherapy. - Source: PubMed
Publication date: 2025/06/18
Li Hong-XingMa Xiao-LingMa Wang-BinJia Tian-YuSun Xiao-HongHe Xiao-XiaZhang Li-LiXi Ya-Ming - Lung adenocarcinoma (LUAD) remains a leading cause of cancer-related mortalities, characterized by substantial genetic heterogeneity that challenges a comprehensive understanding of its progression. This study employs next-generation sequencing data analysis to transform our comprehension of LUAD pathogenesis. Integrating epigenetic and transcriptomic data of LUAD patients, this approach assessed the critical regulatory occurrences, identified therapeutic targets, and offered profound insights into cancer molecular foundations. We employed the DNA methylation data to identify differentially methylated CpG sites and explored the transcriptome profiles of their adjacent genes. An intersectional analysis of gene expression profiles uncovered 419 differentially expressed genes (DEGs) influenced by smoke-induced differential DNA methylation, among which hub genes, including mitochondrial ribosomal proteins (MRPs), and ribosomal proteins (RPs) such as MRPS15, MRPS5, MRPL33, RPL24, RPL7L1, MRPL15, TUFM, MRPL22, and RSL1D1, were identified using a network-based approach. These hub genes were overexpressed and enriched to RNA processing, ribosome biogenesis, and mitochondrial translation, which is critical in LUAD progression. Enhancer Linking Methylation/Expression Relationship (ELMER) analysis revealed transcription factor (TF) binding motifs, such as JUN, NKX23, FOSB, RUNX3, and FOSL1, which regulated these hub genes through methylation-dependent enhancer dynamics. Predominant hypomethylation of MRPs and RPs disrupted mitochondrial function, contributed to oxidative phosphorylation (OXPHOS) and metabolic reprogramming, favoring cancer cell survival. The survival analysis validated the clinical relevance of these hub genes, with high-expression cohorts exhibiting poor overall survival (OS) outcomes enlightened their relevance in LUAD pathogenesis and presented the potential for developing novel targeted therapeutic strategies. - Source: PubMed
Publication date: 2025/03/17
Mukherjee ArnabBoonbangyang ManonK S Mukunthan - Collagen VI-related dystrophies (COL6RD) are a group of rare muscle disorders caused by mutations in specific genes responsible for type VI collagen production. It affects muscles, joints, and connective tissues, leading to weakness, joint problems, and structural issues. Currently, there is no effective treatment for COL6RD; its management typically addresses symptoms and complications. Therefore, it is essential to decipher the disease's molecular mechanisms, identify drug targets, and develop effective treatment strategies to treat COL6RD. In this study, we employed differential gene expression analysis, weighted gene co-expression network analysis, and genome-scale metabolic modeling to investigate gene expression patterns in COL6RD patients, uncovering key genes, significant metabolites, and disease-related pathophysiological pathways. First, we performed differential gene expression and weighted gene co-expression network analyses, which led to the identification of 12 genes (, , , , , , , , , , , ) as potential hub genes involved in the disease. Second, we utilized a drug repurposing strategy to identify pharmaceutical candidates that could potentially modulate these genes and be effective in the treatment. Next, we utilized context-specific genome-scale metabolic models to compare metabolic variations between healthy individuals and COL6RD patients. Finally, we conducted reporter metabolite analysis to identify reporter metabolites (e.g., phosphatidates, nicotinate ribonucleotide, ubiquinol, ferricytochrome C). In summary, our analysis revealed critical genes and pathways associated with COL6RD and identified potential targets, reporter metabolites, and candidate drugs for therapeutic interventions. - Source: PubMed
Publication date: 2024/10/29
Ceyhan Atakan BurakKaynar AliAltay OzlemZhang ChengTemel Sehime GulsunTurkez HasanMardinoglu Adil