MRPS12 antibody
- Known as:
- MRPS12 (anti-)
- Catalog number:
- orb127084
- Product Quantity:
- 5 ug
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- MRPS12 antibody
Related genes to: MRPS12 antibody
- Gene:
- MRPS12 NIH gene
- Name:
- mitochondrial ribosomal protein S12
- Previous symbol:
- RPMS12
- Synonyms:
- RPS12, RPSM12
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-10
- Date modifiied:
- 2016-11-16
Related products to: MRPS12 antibody
Related articles to: MRPS12 antibody
- Microplastics are emerging contaminants that pose health risks. They can cause hepatic lipid interventions, but the underlying mechanisms require investigation. This study assessed the retention of polypropylene microplastics in mouse liver and determined the intercorrelations between hepatic lipid fluctuations and transcriptomic changes. Microplastic-induced liver dysfunction was confirmed by the variations of transamination, cholesterol metabolism, biotransformation, and redox state. Chronic high-dose treatment induced distinct pathological changes, including regional fibrotic remodeling and ultrastructural mitochondrial abnormalities. Raman biospectra of liver slice proposed vital peaks of 1060, 1132, 1168, 1340, 1446, 1618, and 1670 cm, representing the liver biomolecule landscapes. Transcriptomic changes were mainly involved in mRNA transcription, multicellular organism development, various stimuli response, cell differentiation, and lipid metabolic process. Microplastic exposure dosage exerted more profound effects than exposure duration on gene expressions of oxidation-reduction process, signal transduction, and lipid metabolism. WGCNA analysis proposed 47 hub genes involved gene expression orchestration, cell fate monitor, and mitochondria translation modulation. Nine differentially expressed genes associated with lipid biomarkers were related to mitochondria transcription ( and ), cell differentiation , and ), lipid catabolism ( and ) and tRNA methyltransferase (), and Raman peak at 1670 cm intimately connected with aggregated forms of protein. Our findings suggested that polypropylene microplastics could change the liver molecular landscape and induce lipid metabolism disorders and transcriptomic changes in mitochondrial protein translation and expression regulation, highlighting their significant consequences in nutrient and energy imbalance. - Source: PubMed
Publication date: 2025/10/29
Wang MiaoWang JingSun XinglinZhang KenaGao JingXu XiaoyingWu JiaruiTao FangfangZhang DayiLiu Mingying - Scale simplification is a key trend in psychometric research, aiming to reduce the measurement burden while preserving reliability, validity, and applicability. This study aims to develop a more efficient short version of the Malnutrition Risk Perception Scale (MRPS) for older adults by simplifying the original 35-item version (MRPS-35). Genetic algorithms were used to optimize the MRPS-35, resulting in the short MRPS. Reliability, validity, and structural consistency were tested, and measurement invariance across gender groups was assessed, including configural, weak, and strong invariance. The scale was simplified to 12 items (MRPS-12), which demonstrated strong reliability, validity, and structural consistency, showing high comparability to the original MRPS-35. Measurement invariance testing confirmed configural, weak, and strong invariance, indicating the scale's stability across gender groups. As a more efficient assessment tool, the MRPS-12 holds significant potential for community use, enabling the rapid identification of malnutrition risk perception among older adults and supporting tailored nursing interventions. - Source: PubMed
Publication date: 2026/07/10
Wei LanzhiChong Mei-ChanGunarathne Nadeeka Shayamalie - This study investigates the expression and functional significance of mitochondrial ribosomal protein S12 (MRPS12) within NSCLC pathogenesis. The Cancer Genome Atlas dataset reveals a significant association between MRPS12 overexpression and unfavorable clinical outcomes in NSCLC patients. Single-cell RNA sequencing data unequivocally confirm MRPS12 overexpression across diverse NSCLC cancer cell populations. MRPS12 is also upregulated in locally-treated NSCLC tissues. shRNA-mediated gene silencing or CRISPR-Cas9-mediated gene knockout (KO) of MRPS12 impaired mitochondrial function, resulting in a reduction in oxygen consumption rate, marked declines of complex I activity and ATP levels, mitochondrial membrane depolarization, and an increase in reactive oxygen species production in NSCLC cells. Moreover, MRPS12 silencing or knockout attenuated cell viability, proliferation, and migratory capacity, while inducing apoptotic cell death in various NSCLC cell types. Conversely, ectopic MRPS12 overexpression conferred a pro-tumorigenic phenotype to NSCLC cells. In vivo studies demonstrated that MRPS12 silencing markedly inhibited the growth of subcutaneous xenografts derived from primary NSCLC cells in nude mice. The MRPS12-silenced NSCLC xenografts exhibited decreased ATP levels, elevated oxidative injury, diminished proliferation, inhibited Akt-mTOR activation and an increase in apoptosis. These findings support the important role of MRPS12 in supporting mitochondrial function and driving the malignant progression of NSCLC. - Source: PubMed
Publication date: 2025/11/14
Chen ZihaoJin YuWei ShiyouWei RongqiangDing Xinyu - Long noncoding RNA (lncRNA) plays a critical role in cancer cell proliferation, invasion, metastasis, and chemoresistance. The current study introduces novel lncRNAs in colorectal cancer (CRC) through bioinformatics analysis. GSE134834 CRC-related microarray of Gene Expression Omnibus (GEO) was analyzed to identify differentially expressed genes (DEGs) in CRC samples against normal samples. Analysis revealed 6763 DEGs ( < 0.05 and |log fold change (FC)| ≥ 0.5) that include differentially expressed mRNA (DEmRNA) and differentially expressed long noncoding RNA (DElncRNA). Novel lncRNAs were identified, and to better understand the biological function of the identified lncRNAs, gene modules were constructed using weighted gene coexpression network analysis (WGCNA), and finally, two modules for lncRNAs were obtained. The coexpression modules with these lncRNAs were subjected to enrichment analysis in FunRich software to predict their functions through their coexpressed genes. Gene ontology results of modules related to novel lncRNA revealed they significantly enriched the cellular pathways regulation in cancer. The protein-protein interaction (PPI) network of novel lncRNAs-related modules was constructed using Search Tool for the Retrieval of Interacting Genes (STRING) and visualized using the Cytoscape software. Hub genes were screened from the PPI network by the CytoHubba plug-in of Cytoscape. The hub genes were , , , , , , , , , and for the lightpink4 module and , (ribosomal protein S23), (ribosomal L1 domain containing 1), , , , , (nucleolar protein 6), , and (ribosomal RNA processing 12 homolog) for the pink module. The expression levels of the top DEmRNA and module hub genes in CRC were validated using the Gene Expression Profiling Interactive Analysis (GEPIA) database. Generally, our findings offer crucial insight into the hub genes and novel lncRNAs in the development of CRC by bioinformatics analysis, information that may prove useful in the identification of new biomarkers and treatment targets in CRC; however, more experimental investigation is required to validate the findings of the present study. - Source: PubMed
Publication date: 2025/01/29
Heidari RaziehAssadollahi VahidehMarashi Seyedeh NegarElahian FatemehMirzaei Seyed Abbas - Maintaining mitochondrial homeostasis is crucial for cell survival and organismal health, as evidenced by the links between mitochondrial dysfunction and various diseases, including Alzheimer's disease (AD). Here, we report that lncMtDloop, a non-coding RNA of unknown function encoded within the D-loop region of the mitochondrial genome, maintains mitochondrial RNA levels and function with age. lncMtDloop expression is decreased in the brains of both human AD patients and 3xTg AD mouse models. Furthermore, lncMtDloop binds to mitochondrial transcription factor A (TFAM), facilitates TFAM recruitment to mtDNA promoters, and increases mitochondrial transcription. To allow lncMtDloop transport into mitochondria via the PNPASE-dependent trafficking pathway, we fused the 3'UTR localization sequence of mitochondrial ribosomal protein S12 (MRPS12) to its terminal end, generating a specified stem-loop structure. Introducing this allotropic lncMtDloop into AD model mice significantly improved mitochondrial function and morphology, and ameliorated AD-like pathology and behavioral deficits of AD model mice. Taken together, these data provide insights into lncMtDloop as a regulator of mitochondrial transcription and its contribution to Alzheimer's pathogenesis. - Source: PubMed
Publication date: 2024/10/18
Xiong WandiXu KaiyuSun Jacquelyne Ka-LiLiu SilingZhao BaizhenShi JieHerrup KarlChow Hei-ManLu LinLi Jiali