Ask about this productRelated genes to: MRPL47 Blocking Peptide
- Gene:
- MRPL47 NIH gene
- Name:
- mitochondrial ribosomal protein L47
- Previous symbol:
- -
- Synonyms:
- CGI-204, NCM1
- Chromosome:
- 3q26.33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-10-12
- Date modifiied:
- 2014-11-19
Related products to: MRPL47 Blocking Peptide
Related articles to: MRPL47 Blocking Peptide
- MRPL47 (Mitochondrial Ribosomal Protein Large Subunit 47) gene in chromosome 3q26 encodes a protein that is part of the large subunit of the mitochondrial ribosome. We observed that MRPL47 is frequently amplified and overexpressed in ovarian cancer samples. Importantly, increased expression of mRNA is associated with high levels of MRPL47 protein in ovarian cancer patients. High expression of MRPL47 is also associated with poor overall and recurrence free survival of ovarian cancer patients. Notably, MRPL47 improved metabolic fitness by enhancing cellular respiration, and glycolysis in cancer cells. Gene set enrichment analysis and target specific knockdown assays revealed that MYC transcription factor regulates MRPL47 expression. Furthermore, MRPL47 was identified very high in the plasma samples of ovarian cancer patients compared to those of healthy volunteers. MRPL47 was also associated with cisplatin resistance, whereas its expression predicted sensitivity to cisplatin therapy. Taken together, we demonstrated that MRPL47 can be used as a diagnostic biomarker for ovarian cancer and other cancers with 3q26 chromosomal amplification. - Source: PubMed
Publication date: 2026/03/09
Pradeep MeenakshiKadamberi Ishaque PulikkalGeorge JasmineGao YueyingDagum CamillaNair AjayTsaih Shirng-WernGeethadevi AnjaliNair AnupamaHopp ElizabethUyar DeniseBradley WilliamRader JanetLi YongshengChaluvally-Raghavan PradeepOjesina Akinyemi I - In this exploratory pilot study, we profiled human periodontal ligament (PDL) transcriptomes during early orthodontic tooth movement (OTM). Early-stage (0-10 days) transcriptional dynamics under tension and compression remain insufficiently understood, and no dedicated user-friendly resource has been available for exploring large-scale human data. - Source: PubMed
Publication date: 2026/02/18
Zhang XiaoqiXing LuAi-Gumaei WaseemZhang XiaoqianWang QingxuanLi MinqiLong HuLai Wenli - Mitoribosomes are pivotal for cellular energy metabolism through the synthesis of proteins essential for the oxidative phosphorylation system. Although mitoribosomal dysregulation has been implicated in cancer, the genomic landscape of mitoribosomal proteins (MRPs) in nonsmall cell lung cancer (NSCLC) remains largely uncharacterized. In this study, we conducted a comprehensive analysis of expression, copy number variations, and mutations of MRPs using data from TCGA-NSCLC patients. This screen identified MRPL47 as a significantly amplified and overexpressed mitoribosomal gene in NSCLC. Validation across three independent datasets (n = 1513) confirmed MRPL47 as a robust and independent prognostic marker for poor survival. Functionally, MRPL47 inhibition significantly reduced NSCLC cell proliferation and migration. Intriguingly, MRPL47 depletion selectively impaired the translation of a subset of mitochondrial proteins, rather than causing a global defect, leading to impaired assembly of electron transport chain Complexes I and III. This resulted in a defective oxidative phosphorylation system, characterized by decreased ATP synthesis and elevated mitochondrial reactive oxygen species (ROS) levels. Transcriptomic analysis revealed a significant downregulation of E2F pathway activity in MRPL47-knockdown cells, with MRPL47 expression correlating with E2F target gene expression at both RNA and protein levels. Mechanistically, MRPL47 knockdown induced ROS accumulation, which promoted p38 phosphorylation and subsequent upregulation of p21. Increased p21, in turn, led to Rb hypophosphorylation, thereby inhibiting E2F activity and inducing G1 cell cycle arrest and senescence. Altogether, these findings establish that MRPL47 is amplified and overexpressed in NSCLC, functions as a strong prognostic predictor, and critically promotes tumor progression by modulating mitochondrial function and the ROS-p38-p21-Rb-E2F signaling axis. - Source: PubMed
Publication date: 2025/12/15
Bhandari NikitaDevi Yengkhom GhanapriyaAcharya DishaBhat VinitaChatterjee AnneshaYalshetti ShwetaArandkar SharathchandraChaube Bal KrishnaShukla Sudhanshu - Asymptomatic Alzheimer's disease (AsymAD) refers to individuals who, despite exhibiting amyloid-β plaques and tau pathology comparable to Alzheimer's disease (AD), maintain cognitive performance similar to cognitively normal individuals. The resilience mechanism in these AsymAD individual remains understudied. We performed a systematic analysis comparing AsymAD and AD across multiple cohorts (ROSMAP, Banner and Mount Sinai), brain regions (BA6, BA9, BA36 and BA37) and neuronal and glial cell types using proteomics and transcriptomics data. AsymAD brains exhibited preserved mitochondrial bioenergetics, characterized by enhanced oxidative phosphorylation (OXPHOS), electron transport chain (ETC) activity, fatty acid and lipid metabolism, and branched-chain amino acid (BCAA) utilization. Pathways regulating mitochondrial complex biogenesis and calcium homeostasis were also upregulated. Key mitochondrial proteins such as MRPL47, CPT2, BCAT2, and IDH2, were consistently upregulated in AsymAD, whereas MACROD1 was downregulated. At the cellular level, excitatory neurons, including superficial, mid-layer, and deep-layer subtypes, exhibited the most preserved mitochondrial function, whereas vulnerable inhibitory subtypes, including PVALB and SST neurons, showed increased cellular abundance and bioenergetic activity. In contrast, microglia and oligodendrocytes proportions were reduced in AsymAD relative to AD. Our findings identify preserved mitochondrial bioenergetics as a defining feature of resilience in AD and suggest that enhancing NADH metabolism via NAD+ precursor-based interventions may potentially help in maintaining cognitive function despite amyloid and tau pathology. - Source: PubMed
Publication date: 2025/11/06
Mandal PurbaTrushina EugeniaArnold MatthiasKaddurah-Daouk RimaBaloni Priyanka - To investigate the role of mitochondrial ribosomal proteins (MRPs) in the pathogenesis and progression of septic myocardial injury. Additionally, we aim to propose new technical strategies and experimental foundations for the prevention and treatment of septic myocardial injury. - Source: PubMed
Publication date: 2025/02/21
Wu LiuliHuang JunchaoJia XiongfeiMao Xiaoqin