ECHDC2 (C-term) Rabbit antibody Ab
- Known as:
- ECHDC2 (C-terminus) Rabbit (anti-) Antibody
- Catalog number:
- AP17998PU-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- ECHDC2 (C-term) Rabbit antibody
Related genes to: ECHDC2 (C-term) Rabbit antibody Ab
- Gene:
- ECHDC2 NIH gene
- Name:
- enoyl-CoA hydratase domain containing 2
- Previous symbol:
- -
- Synonyms:
- FLJ10948
- Chromosome:
- 1p32.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-12
- Date modifiied:
- 2015-11-11
Related products to: ECHDC2 (C-term) Rabbit antibody Ab
Related articles to: ECHDC2 (C-term) Rabbit antibody Ab
- : This study aimed to identify core genes associated with mitochondria-related transcriptomic signatures and evaluate their potential as computational biomarkers, immune characteristics, regulatory mechanisms, and potential therapeutic relevance. : Obesity-related transcriptome datasets were obtained from the GEO database. Differentially expressed genes (DEGs) were intersected with mitochondria-related genes (MRGs) to identify obesity-related MRGs. Functional enrichment, protein-protein interaction (PPI) analysis, CytoHubba, LASSO and random forest algorithms were used to screen core genes. External validation, ROC analysis, immune infiltration analysis, regulatory network construction, candidate drug prediction, and molecular docking were further performed. : A total of 527 DEGs and 15 differentially expressed MRGs were identified. Enrichment analysis suggested that these mitochondria-related genes were mainly associated with disrupted mitochondrial energy metabolism, lipid metabolic remodeling, and altered substrate utilization. , , , and were identified as core MRGs; these genes are respectively associated with mitochondrial metabolic regulation, de novo fatty acid synthesis, N-acetylaspartate-related mitochondrial metabolism, and lysine degradation. These genes were significantly downregulated in obesity and showed good diagnostic performance. Immune infiltration analysis revealed alterations in the immune microenvironment, and the core genes were negatively correlated with multiple immune cell types. Molecular docking showed that Genistein had the lowest predicted binding free energy with NAT8L (-8.89 kcal/mol), suggesting relatively favorable binding among the tested ligand-target pairs. : , , , and may serve as candidate computational biomarkers, among which represents a known lipid metabolism-related gene, supporting the biological plausibility of the workflow. - Source: PubMed
Publication date: 2026/06/15
Yun HezhangLiu ChangGao BinghongChen Peijie - BACKGROUND: Studies have shown that mitochondrial dysfunction in macrophages worsens inflammation and impedes repair after acute myocardial infarction (AMI). This study aimed to identify and validate biomarkers of AMI associated with mitochondria-related genes (MRGs) and macrophage polarization-related genes (MPRGs), offering new targets and strategies for therapeutic intervention of AMI. METHODS: In this study, the GSE61144 and GSE60993 datasets were employed. Initially, candidate genes were identified by overlapping the differentially expressed genes (DEGs) from differential expression analysis, key module genes from weighted gene co-expression network analysis (WGCNA), and MRGs. Then, biomarkers were identified by machine learing, receiver operating characteristic (ROC), and gene expression analyses. Finally, functional enrichment, immune infiltration, drug prediction, and reverse transcription quantitative polymerase chain reaction (RT-qPCR) analyses were performed to explore the roles of these biomarkers. RESULTS: The study identified APEX1, ECHDC2, NME3, and PUS1 as biomarkers associated with AMI, all of which exhibited reduced expression in AMI samples. RT-qPCR results further validated these findings. Notably, all 4 biomarkers were predominantly co-enriched in the “ribosome” pathway, highlighting its significance in AMI. Additionally, 11 differential immune cells were identified. Correlation analysis revealed that these biomarkers showed the strongest positive correlations with activated CD8 T cells and the most negative correlations with neutrophils. Drug prediction indicated that valproic acid, which targeted all 4 biomarkers, could be a promising therapeutic option for AMI. CONCLUSIONS: In this study, APEX1, ECHDC2, NME3, and PUS1 were identified as biomarkers for AMI, with their expression levels validated in clinical samples. These findings offered a potential theoretical foundation for developing targeted treatments for AMI. CLINICAL TRIAL NUMBER: Not applicable. - Source: PubMed
Publication date: 2026/05/29
Qu NanBai FawenLan Jin - Growing evidence implicates enoyl-CoA hydratase domain-containing protein 2 (ECHDC2) in oncogenesis, yet its role in glioblastoma (GBM) remains undefined. We aimed to clarify the pathological significance and molecular mechanisms of ECHDC2 in GBM. - Source: PubMed
Publication date: 2026/02/09
Lin ShengliangWei TianWu QianLiu QingqingHu LongyunSong BiguiLin JiejingZhao ZeweiCai YiLi XiaoxiaoYang ZhonghanLi ChengmingHu Xiping - Ischemic stroke (IS) is a cerebrovascular disease resulting from insufficient blood supply to specific areas of the brain, often due to atherosclerosis and thrombosis. While the association between polymorphisms in coagulation-related genes (CRGs) and thrombosis has been suggested, the precise relationship between CRGs and IS remains unclear and requires further exploration. - Source: PubMed
Publication date: 2025/12/24
Li HepengLiang JunliLan YuanChen Menghua - Ischemic Stroke (IS) represents the most prevalent subtype of cerebrovascular disease, characterized by complex pathophysiological mechanisms that remain inadequately characterized, particularly concerning mitochondrial dysfunctions. These mitochondrial impairments are increasingly recognized as contributory factors in IS pathogenesis, emphasizing the need for further investigation into the underlying molecular mechanisms involved. - Source: PubMed
Publication date: 2025/10/10
Qi ChaoDong FengYang KaiLv Yanfei