Ask about this productRelated genes to: ECHDC2 antibody
- 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 antibody
Related articles to: ECHDC2 antibody
- 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 - Vitamin D plays a multifaceted role in the body, influencing a wide range of physiological processes. While its benefits in deficiency states are well recognized, the effects of high-dose vitamin D₃ supplementation in vitamin D-sufficient individuals remain poorly understood. In this study, we applied an integrative transcriptomic and proteomic approach to assess the dose-dependent effects of long-term dietary vitamin D₃ supplementation (5000 and 10,000 IU/kg feed) in healthy pigs. Despite the absence of phenotypic alterations in fattening characteristics, we observed significant molecular changes in liver tissue, particularly in pathways related to fatty acid β-oxidation, amino acid catabolism, and oxidative stress response. High-dose vitamin D₃ supplementation led to consistent downregulation of key genes and proteins involved in mitochondrial and peroxisomal β-oxidation, including ACSL5, ACADVL, HADHA, ACAA1 (gene expression), and ACADM, ECHDC1, and ECHDC2 (protein level). These findings suggest a reduced hepatic capacity for activating and degrading long-, very long-, and medium-chain fatty acids, potentially resulting in the accumulation of lipid intermediates and a shift toward alternative metabolic pathways. Our findings indicate that very high-dose vitamin D₃ supplementation in non-deficient states may lead to adverse metabolic shifts in the liver, including lipid accumulation and compromised energy metabolism. These effects appear to be dose-dependent, and while they may not manifest phenotypically in short-lived species, they offer important insights into non-classical toxicological effects of high-dose vitamin D₃ supplementation. Importantly, this study highlights the context-dependent nature of vitamin D's effects and provides a new direction for research focused on its metabolic roles beyond classical pathways. - Source: PubMed
Publication date: 2025/07/16
Steg AnnaSmołucha GrzegorzŚwiątkiewicz MałgorzataOczkowicz Maria