ECHDC2 (C_term)
- Known as:
- ECHDC2 (C_term)
- Catalog number:
- AP17998PU-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- ECHDC2 (C_term)
Related genes to: ECHDC2 (C_term)
- 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)
Related articles to: ECHDC2 (C_term)
- 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 - The mC RNA modifications have been implicated in the pathogenesis of urothelial carcinoma and hold potential as prognostic biomarkers for muscle-invasive bladder cancer (MIBC) patients. In this study, we developed an MIBC-risk model by integrating mC modification-related genes and differentially expressed genes using Nanopore sequencing and a machine learning approach. Compared to our previous research, we observed that mC modifications are more functional, with the most enriched regions being the 3'UTR and exons. Our analysis revealed differential mC methylation sites in several well-characterized cancer-related genes, including BMI1, PTEN, MALAT1, FADD, STAT5A, BIRC6, FOXO3, CCNG1, PAK2, UBE2L3, SMARCB1, and TUG1. Functional enrichment analysis demonstrated significant involvement of these genes in key oncogenic pathways, particularly DNA damage response, double-strand break repair, p53 signaling, MAPK cascade, NF-κB signaling, and cell proliferation/migration pathways. Unlike models based on single factors, the combination of mC modification-related genes and differentially expressed genes resulted in a more effective classification model. This approach yielded an optimized 11-gene prognostic signature comprising GGA1, NUMBL, ECHDC2, NLRC5, EIF2D, GJA1, XPC, DAZAP2, C6orf120, WDR45, and CES1, which demonstrated superior predictive performance in TCGA MIBC patients. These findings establish mC RNA modification patterns as promising molecular signatures for MIBC prognosis and potential therapeutic targets. - Source: PubMed
Publication date: 2025/09/25
Zhang LiliZhou LiyingXu WenruiWu PengjieChen WenLi HexinSun GaoyuanXu SiyuanTang XiaokunLiu LipinZhang YaqunZhong Qiuzi