Ask about this productRelated genes to: PECI antibody
- Gene:
- ECI2 NIH gene
- Name:
- enoyl-CoA delta isomerase 2
- Previous symbol:
- PECI
- Synonyms:
- ACBD2, DRS1, HCA88
- Chromosome:
- 6p25.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-17
- Date modifiied:
- 2016-10-05
Related products to: PECI antibody
Related articles to: PECI antibody
- Studies have shown that substance use liability is associated with novelty seeking, anxiety-like behavior, and pain sensitivity. We examined whether common genetic variation in outbred Sprague-Dawley rats explained variation in behavioral measures from three assays with established links to substance use: locomotor response to a novel environment, elevated plus maze, and tail flick. We estimated single-nucleotide polymorphism heritability and performed genome-wide association analyses using permutation-derived significance thresholds (N=534-654 rats across traits). Heritability estimates ranged from 0.14-0.38 across eleven traits. Three independent loci were identified: chromosome 1 for elevated plus maze open-arm behavior (α=0.05), chromosome 14 for elevated plus maze immobility (α=0.10), and chromosome 17 for tail flick latency (α=0.05). Candidate genes included , , and (chromosome 1); and (chromosome 14); and and (chromosome 17). We compared these loci with our genome wide association study of a F intercross of selectively bred high- and low-responder rats, originally derived from Sprague-Dawleys, that model individual differences in externalizing and internalizing behavior. The current loci are distinct from the ones identified in the bred lines. This difference likely reflects selection history in the high- and low-responder Fs, which focused on facets of exploratory locomotion, while loci for anxiety and pain sensitivity traits were identified in the outbreds. This highlights the benefit of using both outbred and selectively bred rats to probe causal variants contributing to individual differences in substance use liability. The current outbred findings implicate monoaminergic signaling, transcriptional control, and lipid metabolism as testable mechanisms for addiction-relevant behaviors. - Source: PubMed
Publication date: 2026/02/19
Chitre Apurva SHebda-Bauer Elaine KEmery Michael ALi FeiNguyen Khai-MinhWang YizhiCheng RiyanPolesskaya OksanaWatson Stanley JLi JunAkil HudaPalmer Abraham A - Trastuzumab, a cornerstone therapy for HER2-positive breast cancer, is associated with significant cardiotoxicity, manifesting as left ventricular dysfunction and heart failure. This study aimed to identify mitochondrial-related genes pivotal to Trastuzumab-induced cardiotoxicity (TIC) using integrative bioinformatics and machine learning. Analysis of gene expression datasets identified 19 mitochondrial-related differentially expressed genes (MRDEGs), enriched in fatty acid metabolism and oxidative pathways. Machine learning algorithms (LASSO, MCODE, Cytohubba, WGCNA) prioritized four key genes: ACSL1, ECI2, LONP1, and CPT1A. Cross-validation revealed CPT1A as the most consistent biomarker, showing upregulated expression in TIC and strong diagnostic potential (AUC > 0.8). In vivo validation using trastuzumab-treated mice and in vitro cell experiments confirmed CPT1A's dose-dependent upregulation, correlating with impaired cardiac function. Transcriptome sequencing and immune infiltration analysis further linked CPT1A to altered T-cell subsets, suggesting immune-metabolic crosstalk in TIC. In vitro mechanistic studies revealed that CPT1A may promote mitochondrial damage and induce cardiomyocyte injury by interacting with Parkin. This study underscores the utility of multi-omics integration in elucidating TIC mechanisms and paves the way for personalized cardioprotective strategies in HER2-targeted therapy. - Source: PubMed
Publication date: 2025/12/11
Liu YukunChen BinjieLi HanqingZhang WenhaiLian BinHuang ZhenQin QinghongTan QixingWei Chang-Yuan - Yucan granules (YCG) have demonstrated therapeutic benefits in reducing urinary total protein in patients with diabetic kidney disease (DKD); however, their renoprotective mechanisms remain unclear. - Source: PubMed
Publication date: 2025/10/15
Zhang YahengSheng GuangyuZhang ChengjieSong TingYu JingjianRuan WeiXi DerongYu ZhenjieFei WenyiYang Xuejun - Lower back pain caused by intervertebral disk degeneration (IDD) is a common problem among middle-aged and older adults. We aimed to identify novel diagnostic biomarkers of IDD and analyze the potential association between key genes and immune cell infiltration. We screened differentially expressed genes (DEGs) related to IDD and gene sets associated with mitochondrial energy metabolism using the Gene Expression Omnibus and GeneCards databases, respectively. Subsequently, we used multiple enrichment analysis methods to determine the biological functionalities of mitochondrial energy metabolism-related differentially expressed genes (MEMRDEGs). Key genes were selected using logistic regression analysis, a support vector machine algorithm, and least absolute shrinkage and selection operator regression analysis to construct an IDD diagnostic model. To obtain further insights, we examined the relationship between key genes and the presence of infiltrating immune cells. We screened 1304 DEGs that exhibited substantial differences in 20 pathways, including the Wnt signaling pathway, between the IDD and control groups. We identified 33 MEMRDEGs and selected 7 key genes (NDUFA6, YWHAZ, DLAT, BDNF, ECI2, ACO1, and ALDH7A1) to construct an IDD diagnostic model. Receiver operating characteristic curve analysis revealed that these genes exhibited high accuracy in assessing IDD risk, with BDNF and DLAT particularly distinguishing between the low- and high-risk IDD groups. Finally, using single-sample gene set enrichment analysis, we identified a relationship between IDD and immune infiltration, with most immune cells showing strong correlations. A significant positive relationship was found between ACO1 and the immune cells, known as immature dendritic cells. These results offer remarkable insights into the mechanisms underlying the occurrence and development of IDD, potentially identifying new opportunities for diagnosis and therapeutic intervention. - Source: PubMed
Lv JianlanWang Zhenwei - Mitochondrial function plays a crucial role in understanding the pathogenesis of acute myocardial infarction.This study investigates mitochondrial function-related genes (MFRGs) in acute myocardial infarction (AMI) through bioinformatics and rigorous experimental validation. Using three integrated GEO datasets (149 samples: 80 AMI, 69 control), we applied machine learning methods (Random Forest, Support Vector Machine, Least Absolute Shrinkage and Selection Operator), phenotype scoring, consensus clustering, and weighted gene co-expression network analysis in three subgrouping stages to refine the selection of MFRGs. The intersection of three subgroup analyses results identified 11 key Mitochondrial function-Related Differentially Expressed Genes (MRDEGs). Gene Ontology / Kyoto Encyclopedia of Genes and Genomes analysis (GOKEGG), Gene Set Enrichment Analysis (GSEA), Gene Set Variation Analysis (GSVA), and immune infiltration analyses revealed significant pathways and suggested alterations in the composition of immune cell subpopulations. Single-cell analysis revealed increased expression of MRDEGs (NDUFA8, ECI2, and ACADM) in cardiomyocytes, fibroblasts, and macrophages, along with dynamic expression trends along the pseudotime trajectory. Subgroup analysis of cardiomyocytes based on mitochondrial gene scoring was performed to explore functional enrichment characteristics. Furthermore, we robustly validated these genes' expression in the cardiomyocyte hypoxia/reoxygenation model and the mouse model of myocardial infarction using flow cytometry, immunohistochemistry, and Western blot. Finally, this study constructed the mRNA regulatory network of key MRDEGs and preliminarily explored the potential therapeutic value of valproic acid and acetaminophen through molecular docking.These findings reveal the role of mitochondrial dysfunction in the mechanisms of AMI and its associated cell subpopulations, along with the involved biological pathways, offering new insights for AMI research. - Source: PubMed
Publication date: 2025/07/05
Hao YingFan ChengHuiWen WeiLi RuiLinGao YangHou XiaLu LinxiangShen YunLi