Ask about this productRelated genes to: MRPL21 antibody
- Gene:
- MRPL21 NIH gene
- Name:
- mitochondrial ribosomal protein L21
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-01-26
- Date modifiied:
- 2014-11-19
Related products to: MRPL21 antibody
Related articles to: MRPL21 antibody
- Neuroblastoma (NB) is the most common extracranial solid tumor in early childhood and frequently presents with bone marrow (BM) metastasis, particularly in high-risk cases. Metastatic NB cells residing in the BM exhibit distinct biological behaviors and are closely associated with treatment resistance and poor prognosis. Emerging evidence suggests that metabolic reprogramming is a hallmark of NB progression; however, its regulatory landscape within the bone marrow microenvironment remains poorly understood. This study aimed to systematically elucidate the molecular mechanisms underlying metabolic reprogramming in bone marrow-infiltrating metastatic NB cells by integrating single-cell transcriptomic data, bulk RNA-sequencing profiles, and in vitro functional validation. Single-cell RNA-sequencing data from 17 bone marrow aspirates of NB patients-with and without marrow infiltration-were retrieved from the GEO database, while bulk RNA-seq data from 155 NB tumor samples were obtained from the TARGET database. A suite of bioinformatics tools, including Seurat, Harmony, CellChat, and SCENIC, was employed to perform multi-dimensional analyses such as cell subtype annotation, intercellular communication mapping, and transcription factor regulon construction. AUCell scoring, differential gene expression analysis, random survival forest modeling, and Kaplan-Meier survival analysis were conducted to identify key genes involved in metabolic reprogramming and to characterize their immune infiltration features. Gene Set Enrichment Analysis (GSEA), Gene Set Variation Analysis (GSVA), and single-cell pathway scoring were applied to predict the metabolic and immune pathways associated with these candidate genes. Furthermore, co-expression network analysis was used to evaluate the relationships between candidate genes and known NB regulatory factors. Finally, in vitro experiments were carried out to validate the roles of selected genes in regulating NB cell proliferation, migration, invasion, and mitochondrial function. Single-cell transcriptomic analysis of bone marrow-derived NB samples identified nine distinct cell subpopulations with diverse intercellular communication networks. Among these, the ligand-receptor pair MDK-NCL emerged as a key mediator of cell-cell signaling. Regulatory network analysis revealed five critical regulons-JUND, JUNB, FOS, E2F1, and KLF16-closely associated with metabolic reprogramming in NB. The "Neuroblastoma cell" cluster displayed markedly elevated metabolic activity. Through integrated analyses, five core metabolic reprogramming genes (MRPL21, NHP2, RPL13, RPL18A, and RPL27A) were identified and shown to be significantly associated with poor prognosis. High expression of these genes correlated with an immunosuppressive tumor microenvironment, characterized by reduced infiltration of monocytes, M1 macrophages, and T cells. Functional enrichment analysis revealed that these genes were primarily enriched in oxidative phosphorylation, MYC targets, PI3K-Akt, and p53 signaling pathways. Co-expression network analysis further demonstrated that MRPL21 and NHP2 positively correlated with known NB regulatory genes TP53, NRAS, and NKIF1B. In vitro assays confirmed that MRPL21 knockdown significantly impaired NB cell proliferation, migration, invasion, and mitochondrial oxidative phosphorylation. This study identified five key genes involved in metabolic reprogramming of bone marrow-infiltrating NB cells, which are closely associated with immunosuppressive microenvironment formation and enrichment in tumor-associated metabolic pathways. Among these, MRPL21 plays a pivotal role in regulating NB cell proliferation and mitochondrial function, underscoring its potential as a promising therapeutic target. These findings suggest that integrated strategies targeting both tumor metabolism and the immune microenvironment may provide new avenues for the treatment of high-risk, metastatic NB. - Source: PubMed
Publication date: 2025/08/05
Chu JingQin RongWang Shu-JingWang QiangWu Qiang - Gestational diabetes mellitus (GDM) is a common pregnancy-related disorder with potential impacts on the fetoplacental unit. To uncover the underlying molecular mechanisms, we conducted a comprehensive bioinformatics analysis using a dataset from Gene Expression Omnibus, which included 37 primary human fetoplacental vascular endothelial cells (FPVEs) from healthy and GDM-complicated pregnancies. We identified 613 differentially expressed genes (DEGs) through the limma package, with 260 up-regulated and 353 down-regulated. Weighted gene co-expression network analysis was then performed, clustering genes into 11 modules. The MEdarkgreen module, containing 1,391 co-expression genes, showed the highest correlation with FPVE programming. After intersecting with DEGs, 192 co-expression hub genes were obtained. Gene Ontology enrichment analysis of these hub genes revealed enrichment in biological processes such as ribonucleoprotein complex biogenesis and ncRNA processing. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed significant enrichment in pathways related to ribosome function, neurodegenerative diseases, and oxidative phosphorylation. Protein-protein interaction network analysis led to the identification of five signature genes (RPS13, MRPS5, MRPL22, MRPL21, and NDUFS3). These genes exhibited significantly lower expression in FPVEs from GDM pregnancies and demonstrated excellent diagnostic performance, with high area under the curve values in receiver operating characteristic analysis. Further KEGG signaling pathway analysis elucidated the multiple signaling pathways in which these signature genes are involved under GDM conditions. We also constructed LncRNA-miRNA-target genes interaction networks for the signature genes. The networks showed that the expression of these genes is regulated by multiple miRNAs and LncRNAs, highlighting the complex post-transcriptional regulatory mechanisms at play. Overall, our study provides novel insights into the molecular basis of FPVE programming in GDM and potential biomarkers for its diagnosis and understanding. - Source: PubMed
Publication date: 2025/07/14
Liu ChunhongWei CaichengLu YulanChai FuWang ChunfangZeng YonglongHuang Huatuo - Head and neck squamous cell carcinoma (HNSCC) constitutes a major clinical challenge that severely affects patient survival. Mitochondrial ribosomal protein (MRP) family plays an important role in energy metabolism by participating in mitochondrial oxidative phosphorylation. However, their roles in HNSCC and the underlying mechanisms are still unclear. - Source: PubMed
Publication date: 2025/07/26
Guan RuiLi CeJiao RuijieLi JingaoWei RanFeng ChenCao ShengdaQian YeFang JugaoLiu JunLi WenmingWei DongminLei Dapeng - The plasma proteins are an important source of therapeutic targets. This study aims to address the diagnostic and therapeutic challenges of bladder cancer (BC) by using Mendelian randomization (MR) with a large sample size from multiple centers to identify the plasma proteins which are causally related to the pathogenesis of BC. Followed by merging nine plasma protein datasets from six studies, a total of 5538 plasma proteins and three BC datasets (ieu-b-4874, ukb-b-8193, FinnGen_R11_C3_ BLADDER_EXALL) were used to perform proteome‑wide MR to estimate the contribution of plasma proteins to BC, separately. To ensure the robustness of the results, Veen intersection operation on MR results revealed that 14 meaningful candidate pathogenic plasma proteins (ANKRD27, BIN1, FAHD1, IL17RB, MRPL21, PPT1, PSCA, SLC16A3, SLURP1, SPON2, TACSTD2, TMEM87B, YWHAB) were obtain from three datasets. Then, we validated these proteins through various methods, including meta-analysis, reverse MR, Bayesian co-localization analysis and summary-data-based MR (SMR), and pathogenic plasma proteins were divided into three layers according to the validation confidence. We then performed single-cell transcriptome analysis (Registration number: GSE222315), which showed that 13/14 candidate plasma proteins were expressed and 12 proteins were differentially expressed in at least one cell type. Finally, protein-protein interactions (PPI) analysis and druggability evaluation were performed to explore the relationship between the interaction of plasma protein markers and existing cancer drug targets. Summarily, our research uncovered 14 plasma protein biomarkers linked to BC risk, offering novel perspectives on the etiology and potential targets for developing screening biomarkers and therapeutic drugs for BC. - Source: PubMed
Publication date: 2025/05/02
Cao JinlongChen SiyuWang JirongFan XinpengLiu ShanhuiShan JiaqiLi XiaoranYang Li - Parkinson's disease (PD) is an age-related and progressive neurodegenerative disease. Growing evidences indicate that CD4 T cell dysfunction plays an essential role in the progress of PD. Here, in LPS-induced PD mice, we isolated midbrain CD4 T cell and peripheral CD4 T cell to perform proteomics, and then screened a total of 167 co-expression proteins via integrated bioinformatics analysis. In addition, the subcellular localization, GO analysis, KEGG pathways and protein-protein interaction of 167 co-expression proteins were assessed. Furthermore, GeneMANIA searched the hub proteins and their co-expression genes and found 13 overlapping hub proteins, including Ndufa3, Cox5b, Mrpl21, Ndufab1, Idh3g, Ndufb7, Cyc1, Cisd1, Atp5f1c, Sdhc, Ndufb9, Mtnd1 and Mrpl17. Next, GO analysis and KEGG analysis of the 13 overlapping hub proteins were also exhibited. Further analysis identified that 4 hub proteins (Idh3g, Cisd1, Atp5f1c and Mtnd1) were downregulated both in midbrain and peripheral CD4 T cell from proteomics. Identification and rescue experiment analysis showed that only Atp5f1c was decreased in LPS- and 6-OHDA-induced PD mice and dopamine (DA) neuronal loss and ATP production decrease were disappeared after Atp5f1c over-expression/Atp5f1c reinfusion both in vivo and in vitro. In conclusion, Atp5f1c was verified as a potential CD4 T cell-related hub protein for PD. - Source: PubMed
Publication date: 2025/01/13
Wang GuoqingWang YuanyuanTang XianjinLi DaidiZhao YujiaZhang Feng