Ask about this productRelated genes to: Mrps33 antibody
- Gene:
- MRPS33 NIH gene
- Name:
- mitochondrial ribosomal protein S33
- Previous symbol:
- -
- Synonyms:
- CGI-139
- Chromosome:
- 7q34
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-20
- Date modifiied:
- 2015-08-25
Related products to: Mrps33 antibody
Related articles to: Mrps33 antibody
- Alzheimer's disease (AD) exhibits sex-specific molecular signatures that may improve diagnostic precision. We aimed to identify and validate male- and female-specific blood and brain gene expression biomarkers for AD prediction. We analyzed four GEO datasets (blood- and brain-derived) using limma and Fisher's meta-analysis to identify sex-specific differentially expressed genes, assessed age associations via linear regression, and constructed 10-fold cross-validated logistic regression models. After performing a meta-analysis, 74 differentially expressed genes were identified in the female cohort and 89 DEGs were screened in the male cohort. ERH and MRPS33 were identified as the most relevant genes in the male cohort, and NDUFA1 and NDUFS5 were screened in the female cohort. The identified genes were downregulated in AD samples compared to controls. Both male-specific and female-specific prediction models achieved an AUC of above 0.7 in two external validation blood-derived datasets as well entorhinal cortex dataset. Paradoxically, qPCR showed significant upregulation of all four genes in the AD group compared to the control group. - Source: PubMed
Publication date: 2026/01/30
Ma XiaomengIbrahim Abdilahi AbdiMa LiliMa XueyingMa ZhanLiu YingyingLi DonghongLiu JiaXu XiaofengDong HuiminChen XiaohongPeng Fuhua - Diabetic retinopathy is a leading cause of blindness in diabetic patients, with disease susceptibility influenced by both genetic and environmental factors. This study aimed to identify novel genetic variants associated with DR and evaluate interactions between polygenic risk scores (PRS) and lifestyle factors in a Korean diabetic cohort. After excluding subjects with non-diabetic retinopathy eye diseases (n = 2519), we analyzed data from 50,361 non-diabetic controls, 4873 diabetic participants without retinopathy (DM-NR), and 165 with diabetic retinopathy (DM-DR). We conducted genome-wide association studies comparing DM-NR and DM-DR groups, performed generalized multifactor dimensionality reduction (GMDR) analysis for epistatic interactions, developed unweighted PRS models, and examined PRS-lifestyle interactions using two-way analysis of covariance. DM-DR prevalence showed strong associations with metabolic syndrome and its components. Five novel genetic variants were identified: _rs17110929, _rs2576531, _rs557869288, _rs1533933, and _rs4936270. A significant three-way epistatic interaction among the first three variants was discovered through GMDR analysis. High-PRS individuals (scores 5-6) showed a 49-fold higher odds ratio of DM-DR compared to low-PRS individuals (scores 0-2; < 0.0001). MAGMA analysis revealed enrichment in pathways related to protein degradation, vascular function, and neuronal signaling, with predominant upregulation in brain tissues. Significant PRS × lifestyle interactions were identified for fruit intake, coffee consumption, alcohol intake, eating duration, and physical activity, with lifestyle factors modifying genetic risk effects (all < 0.003). These findings identify novel genetic variants and epistatic interactions in DM-DR pathogenesis, supporting the use of PRS-based risk stratification for intensive monitoring and personalized lifestyle interventions. The discovery of brain tissue-enriched pathways suggests DM-DR shares mechanisms with neurodegenerative diseases, expanding therapeutic targets beyond traditional vascular approaches. - Source: PubMed
Publication date: 2025/09/17
Park SunminKang SunaJee Donghyun - : Genes and environments were transmitted across generations. Parents' genetics influence the environments of their offspring; these two modes of inheritance can produce a genetic nurture effect, also known as indirect genetic effects. Such indirect effects may partly account for estimated genetic variance in T2D. However, the well-established specific genetic risk factors about genetic nurture effect for T2D are not fully understood. This study aimed to investigate the genetic nurture effect on type 2 diabetes and reveal the potential underlying mechanism using publicly available data. : Whole-genome genotyping data of 881 offspring and/or their parents were collected. We assessed SNP-level, gene-based, and pathway-based associations for different types of genetic effects. : Rs3805116 (β: 0.54, = 4.39 × 10) was significant for paternal genetic nurture effects. ( = 1.58 × 10), ( = 6.76 × 10), and ( = 2.67 × 10) revealed significantly positive paternal genetic nurture effects. Five ontologies were identified as enrichment in both direct and indirect genetic effects, including flavonoid metabolic process and antigen processing and presentation via the MHC class Ib pathway. Two pathways were only enriched in paternal genetic nurture effects, including the transforming growth factor beta pathway. Tissue enrichment of type 2 diabetes-associated genes on different genetic effect types was performed using publicly available gene expression data from the Human Protein Atlas database. We observed significant gene enrichment in paternal genetic nurture effects in the gallbladder, smooth muscle, and adrenal gland tissues. : , , and are associated with increased T2D risk through the environment influenced by paternal genotype, suggesting a novel perspective on paternal contributions to the T2D predisposition. - Source: PubMed
Publication date: 2025/01/07
Li XiaoyiZhou ZechenMa YujiaDing KexinXiao HanWu TaoChen DafangWu Yiqun - To identify novel candidate genes whose expression is associated with bone mineral density (BMD) and body lean mass (LM) in children. - Source: PubMed
Publication date: 2022/12/27
Xu JiawenMa JunZeng YiSi HaiboWu YuangangZhang ShaoyunShen Bin - Mitochondrial ribosomal small subunit (MRPS) group of proteins is structural constituents of the small subunit of mitoribosomes involved in translation. Recent studies indicate role in tumourigenic process, however, unlike cytosolic ribosomal proteins, knowledge on the role of MRPS proteins in alternate cellular processes is very limited. Mapping protein-protein interactions (PPIs) onto known cellular processes can be a valuable tool to identify novel protein functions. In this study, to identify PPIs of MRPS proteins, we have constructed 31 glutathione-S-transferase (GST)/MRPS fusion clones. GST/MRPS fusion proteins were confirmed by MALDI-TOF analysis. GST pull-downs were performed using eight GST/MRPS proteins (MRPS9, MRPS10, MRPS11, MRPS18B, MRPS31, MRPS33, MRPS38 and MRPS39), GST alone as pull-down control and HEK293 cell lysate as the source for anchor proteins followed by nLC/MS/MS analysis and probable PPIs of eight MRPS proteins were identified. Three PPIs from GST pull-downs and interaction between six MRPS proteins and p53 previously reported in PPI database were validated. The PPI network analysis revealed putative role in cellular processes with implications for tumourigenesis. Gene expression screening of a cancer cell line panel indicated overexpression of MRPS10 and MRPS31 in breast cancer. Co-expression module identification tool analysis of breast cancer gene expression and MRPS10 and MRPS31 PPIs revealed putative role for PPI with acyl-CoA dehydrogenase in fatty acid oxidation process regulated by brain-derived neurotrophic factor signalling pathway. - Source: PubMed
Revathi Paramasivam OviyaGopisetty GopalSubramani JayaveluThangarajan Rajkumar