ECH1 Antibody
- Known as:
- ECH1 Antibody
- Catalog number:
- GWB-MP522I
- Product Quantity:
- 100ug
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- ECH1 Antibody
Related genes to: ECH1 Antibody
- Gene:
- ECH1 NIH gene
- Name:
- enoyl-CoA hydratase 1
- Previous symbol:
- -
- Synonyms:
- HPXEL
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-04-26
- Date modifiied:
- 2016-10-05
Related products to: ECH1 Antibody
Related articles to: ECH1 Antibody
- Obesity, a complex metabolic disease, is tightly linked to lipid metabolism disorders. Jinhua Citrus medica Ethanol Extract (CMEE), a substance derived from a food-medicinal source, exhibits significant lipid-lowering and antioxidant properties; however, its systematic mechanisms of action remain incompletely elucidated. This study explored CMEE's anti-obesity and antioxidant mechanisms using a high-glucose-induced Caenorhabditis elegans (C. elegans) model. Network pharmacology predicted that the key mechanisms of CMEE involved the AMPK and PPAR signaling pathway. CMEE treatment notably reduced lipid accumulation levels, extended C. elegans lifespan, and enhanced antioxidant capacity. Mechanistically, CMEE was found to concertedly regulate lipid homeostasis through dual pathways. It activated the AMPK pathway (via aak-2) and upregulated the nuclear receptor NHR-49, thereby promoting the expression of key β-oxidation genes (acs-2, ech-1.1, cpt-1, cpt-2) to enhance fatty acid breakdown. Concurrently, it inhibited the MDT-15/SBP-1 pathway, downregulating desaturase genes (fat-5, fat-6, fat-7) to suppress fat synthesis. Combining network pharmacology, transgenic C. elegans fluorescence assays, and key gene mutant validation, this study established a complete evidence chain from prediction to verification. It clarified CMEE's multi-target role in ameliorating obesity and related metabolic disorders, providing theoretical and experimental support for its development as a functional food. - Source: PubMed
Zhao FujieShi GuilingLiu RuiXu ZheJiang YumeiWang YurongZhang XiaohanWang Hao - Pancreatic cancer remains one of the most lethal malignancies, characterised by aggressive progression, metabolic adaptation, and resistance to therapy. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has emerged as a critical mechanism influencing tumour survival and therapeutic response. However, the role of ferroptosis suppressor genes (FSGs) in pancreatic cancer remains incompletely understood. In this study, FSGs were systematically retrieved from FerrDb V2 and subjected to multi-step filtering to identify a curated set of 196 protein-coding genes. Genomic alteration analysis using cBioPortal across 21 pancreatic cancer studies (n = 5189 samples) identified seven recurrently altered genes (TP53, HSF1, PARP10, ZFP36, SIRT2, ECH1, and ENPP2) with alteration frequencies ≥ 3%. Co-occurrence analysis revealed predominantly cooperative alteration patterns among these genes, suggesting functional complementarity. Survival analysis demonstrated that alterations in FSGs were significantly associated with reduced overall survival in pancreatic cancer, with several genes (ECH1, ZFP36, SIRT2, and ENPP2) showing particularly strong adverse prognostic effects. In contrast, no significant survival associations were observed in oesophageal and gastric cancers, indicating a tumour-specific dependency on ferroptosis-related mechanisms. KEGG pathway enrichment analysis of the broader FSG set revealed significant involvement in pathways related to metabolic regulation (AMPK-mTOR signalling), autophagy, hypoxia response (HIF-1 signalling), and oncogenic signalling (PI3K-Akt pathway). Integration of these findings suggests that ferroptosis suppressor genes contribute to pancreatic cancer progression by promoting metabolic adaptation and resistance to oxidative stress. In conclusion, this study identifies key ferroptosis suppressor genes with prognostic relevance in pancreatic cancer and highlights their integration within critical metabolic and stress-response pathways. The tumour-specific nature of these associations underscores the importance of biological context and supports the potential of FSGs as prognostic biomarkers and potential therapeutic targets in ferroptosis-based strategies. - Source: PubMed
Publication date: 2026/06/10
Singh Nitin KumarSingh ManinderHusain AdilAlnajjar Lina IAhmad FirozMishra Siddhartha KumarAlshamamri NawafSaeed MohdRab Safia ObaidurGupta Varsha - Chromophobe renal cell carcinoma (ChRCC) is characterized by the accumulation of abnormal mitochondria, a high rate of mitochondrial DNA (mtDNA) mutations, and altered oxidative metabolism. There are no existing circulating biomarkers to distinguish metastatic ChRCC from clear cell renal cell carcinoma (ccRCC). - Source: PubMed
Publication date: 2026/03/23
Steiner ClaraHan TiegangSafi StevenBzeih WafaaMansour HadiSaad EddyWilliams Jessica FHirsch Michelle SGiri Vinay KAscione LilianaElon YehonatanDicker Adam PTang YanChoueiri Toni KHenske Elizabeth PXu Wenxin - Zearalenone, a mycotoxin commonly detected in food and the environment, is an underestimated global public health concern, especially as climate change may worsen its prevalence and effects. Although zearalenone has been associated with various adverse health outcomes, the exact mechanistic links to obesogenic effects, mitochondrial dysfunction, and related molecular pathways remain unclear. This research explored the impact of early-life zearalenone exposure on lipid accumulation and its potential relationship to mitochondrial dysfunction in the nematode Caenorhabditis elegans. Multiple lipid indicators, including Nile Red, Oil Red O, lipid droplet-associated fluorescent protein DHS-3, and triglyceride assays, showed that zearalenone exposure (0.3-50 μM) significantly increased worm lipid content. At 50 μM, zearalenone significantly upregulated lipogenesis genes (fasn-1, fat-6, fat-7, pod-2), β-oxidation genes (acs-2, ech-1), and transcription factors (nhr-49, sbp-1). Oil Red O assays using nhr-49 and sbp-1 mutant backgrounds revealed their essential roles in zearalenone-induced obesogenic effects. Exposure to 50 μM zearalenone significantly decreased mitochondrial content, potentially linked to upregulation of the mitochondrial fission gene drp-1. Oil Red O assays using drp-1 RNAi worms suggested that zearalenone's obesogenic effects depended on drp-1. Molecular docking analysis indicated possible spontaneous binding of zearalenone to DRP-1 and its homologues across species. This study offers mechanistic insights into the obesogenic effects of early-life zearalenone exposure, involving interconnected lipid metabolism (sbp-1 and nhr-49) and mitochondrial fission (drp-1), both of which are evolutionarily conserved. - Source: PubMed
Publication date: 2026/03/05
How Chun MingChan Ya-ChinWei Chia-Cheng - Diabetic cardiomyopathy (DCM) is a major cardiovascular complication of diabetes mellitus, ultimately progressing to heart failure and increased mortality. Its pathogenesis involves multifactorial mechanisms, and the key causative genes remain to be fully elucidated. - Source: PubMed
Publication date: 2026/02/17
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