COX4I1 Mouse Monoclonal Antibody
- Known as:
- COX4I1 Mouse Monoclonal Antibody
- Catalog number:
- BIN-001327-M08
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- COX4I1 Mouse Monoclonal Antibody
Related genes to: COX4I1 Mouse Monoclonal Antibody
- Gene:
- COX4I1 NIH gene
- Name:
- cytochrome c oxidase subunit 4I1
- Previous symbol:
- COX4
- Synonyms:
- COX4-1
- Chromosome:
- 16q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-02-11
Related products to: COX4I1 Mouse Monoclonal Antibody
Related articles to: COX4I1 Mouse Monoclonal Antibody
- Fatty liver hemorrhagic syndrome (FLHS) is a nutrition-related metabolic disorder in laying hens characterized by excessive hepatic lipid accumulation and hemorrhagic lesions, leading to reduced productivity and increased mortality. However, the regulatory mechanisms linking mitochondrial dysfunction to hepatic lipid metabolism remain unclear. This study investigated the role of SIRT3 in modulating mitochondrial fatty acid oxidation during FLHS progression. An in vivo FLHS model was established by feeding laying hens with a high-energy, low-protein (HELP) diet, and an in vitro hepatic steatosis model was induced by free fatty acid (FFA) treatment in primary hepatocytes. Both models exhibited pronounced lipid accumulation in hepatic cells and altered hepatocellular injury-related parameters, which were associated with mitochondrial dysfunction and impaired fatty acid oxidation. Mechanistically, hepatic tissues and hepatocytes showed suppression of the SIRT3-AMPKα-PGC-1α signaling cascade, accompanied by reduced expression of mitochondrial biogenesis markers (NRF1, TFAM), impaired respiratory chain components (NDUFA9, SDHA, UQCRC1, COX4I1, ATP5B), and decreased transcription of fatty acid oxidation-related genes (PPARα, ACOX1, CPT1A, CPT2, ACADL, ACADM). Pharmacological activation of SIRT3 with AR-C17 restored AMPKα-PGC-1α signaling, enhanced mitochondrial biogenesis and respiratory function, and promoted fatty acid oxidation, thereby alleviating lipid accumulation in hepatocytes in both models. Collectively, these results demonstrate that SIRT3 is a key metabolic regulator maintaining mitochondrial oxidative function and lipid homeostasis in laying hens. Targeted activation of SIRT3 may provide a novel nutritional strategy for preventing or ameliorating FLHS and related metabolic disturbances in poultry production. - Source: PubMed
Publication date: 2026/04/07
Cao PanpanChen JinyanZeng ChunHu YangYuan JianyunGuo XiaoquanCao HuabinZhang CaiyingZhuang YuHu Guoliang - Airborne particulate matter with a diameter of <10 μm (PM) can damage the corneal epithelium by inducing oxidative stress, disrupting the NRF2 antioxidant pathway, and triggering epithelial barrier dysfunction and inflammation. However, the role of mitochondria in mediating PM-induced damage remains unexplored. This study investigated the impact of PM on mitochondrial homeostasis in both immortalized human corneal epithelial cells (HCE-2) and the mouse corneal epithelium, as well as the protective effects of SKQ1. For in vivo assessment, female C57BL/6 mice were exposed to either control air or PM (±SKQ1) in a whole-body exposure chamber for 2 weeks (3 h/day, 5 days/week, with weekends off). In vitro, HCE-2 cells were exposed to 100 μg/mL PM (±SKQ1) for 24 h, and mitochondrial function and morphology were evaluated. In vitro, PM significantly impaired mitochondrial function by reducing basal, maximal, and ATP-linked respiration; reserve capacity; and coupling efficiency compared to the control and SKQ1 groups. PM also downregulated mitofusin1 (MFN1) and optic atrophy1 (OPA1) and upregulated dynamin-related protein1 (DRP1) and mitochondrial fission protein1 (FIS1) in HCE-2 cells. In addition, PM exposure significantly decreased the mitochondrial membrane potential; mitochondrial DNA copy number; and cytochrome c oxidase subunit 4 isoform 1 (COX4i1), mitochondrial transcription factor A (TFAM), and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) levels. SKQ1 pre-treatment significantly attenuated these effects. In vivo, PM exposure significantly decreased the levels of MFN1, TFAM, COX4i1, and superoxide dismutase (SOD2), whereas SKQ1 treatment significantly reversed these effects. Overall, these findings demonstrate that PM exposure induces mitochondrial fragmentation, disrupts mitochondrial biogenesis and quality control, and reduces mitochondrial respiration, resulting in mitochondrial dysfunction. SKQ1 effectively reversed these changes, suggesting its potential as a therapeutic strategy to protect corneal epithelial cells from PM-induced mitochondrial damage. - Source: PubMed
Publication date: 2026/02/25
Somayajulu MallikaWright RobertMuhammed Farooq SMcClellan Sharon AIbrahim Ahmed SHazlett Linda D - To determine whether maternal tocotrienol-rich fraction supplementation restores mitochondrial-volume, -fusion, and -interaction with lipid droplets in 2-cell embryos of ovalbumin-induced allergic asthma mice. - Source: PubMed
Publication date: 2026/03/14
Wafriy Che IsmailKamsani Yuhaniza ShafinieMuid Suhaila AbdSarbandi Mimi SophiaNor-Ashikin Mohamed Noor Khan - Medulloblastoma (MB) is a common central nervous system malignancy in children, and its relationship with lactate metabolism has become an important area of cancer research in recent years, especially in metabolic reprogramming. This study aimed to determine the effects of lactate metabolism-related genes in the biological mechanisms involved in MB. - Source: PubMed
Publication date: 2026/02/25
Wang CeZhang RongLi ShenglanKang ZhuangXia ShaohuaiLi Wenbin - Renal cell carcinoma (RCC) is characterized by dysregulated lipid metabolism and a high propensity for developing resistance to targeted therapies. Mitophagy is a key process involved in the progression of various cancers, including RCC. Here, using genome-wide CRISPR screening, we identified PRKAB2 as a crucial tumor suppressor in RCC. Reduced PRKAB2 expression correlated with poor prognosis and aggressive clinical features, whereas overexpression of PRKAB2 markedly inhibited RCC cell proliferation, migration, invasion, tumor growth, and metastasis both and . Mechanistically, PRKAB2 overexpression inhibited mitophagy primarily through two distinct mechanisms. First, PRKAB2 enhanced the binding between LRPPRC and PRKN/parkin, competitively reducing PRKN's interaction with PINK1 and thus suppressing ubiquitin-dependent mitophagy. Second, PRKAB2 promoted AMPK phosphorylation, which in turn suppressed SREBF1/SREBP1-mediated transcriptional activation of , leading to decreased CRLS1 expression and reduced synthesis of cardiolipin, a lipid essential for mitophagy. Importantly, PRKAB2 overexpression significantly restored sensitivity to tyrosine kinase inhibitors (TKIs) in sunitinib-resistant RCC cells. Conversely, forced PRKN expression promoted resistance to these drugs, further implicating mitophagy as a key mechanism underlying TKI resistance. Depmap analysis confirmed the association between increased mitophagy and TKI resistance. Overall, our findings identify PRKAB2 as a critical tumor suppressor in RCC, regulating both protein-protein interactions and lipid metabolism to suppress mitophagy. Targeting PRKAB2-associated pathways may provide a promising therapeutic strategy to enhance treatment efficacy and overcome drug resistance in RCC.: ACACA/ACC1: acetyl-CoA carboxylase alpha; AMPK: AMP-activated protein kinase; ATCC: American Type Culture Collection; ATP5F1A: ATP synthase F1 subunit alpha; BNIP3: BCL2 interacting protein 3; BNIP3L/NIX: BCL2 interacting protein 3 like; BRCA1: BRCA1 DNA repair associated; Cas: CRISPR-associated; CCCP: carbonyl cyanide m-chlorophenyl hydrazone; ccRCC: clear cell renal cell carcinoma; ChIP: chromatin immunoprecipitation; Co-IP: co-immunoprecipitation; COX4I1: cytochrome c oxidase subunit 4I1; CRISPR: clustered regularly interspaced short palindromic repeats; CRLS1: cardiolipin synthase 1; DNM1L/DRP1: dynamin 1 like; DOX: doxorubicin; FUNDC1: FUN14 domain containing 1; HSPA8: heat shock protein family A (Hsp70) member 8; HSPD1: heat shock protein family D (Hsp60) member 1; GO: gene ontology; IHC: immunohistochemistry; IMM: inner mitochondrial membrane; LDLR: low density lipoprotein receptor; m-SREBF1: mature sterol regulatory element binding transcriptional factor 1; LRPPRC: leucine rich pentatricopeptide repeat containing; MAP1LC3B: microtubule associated protein 1 light chain 3 beta; MFN1, mitofusin 1; MFN2: mitofusin 2; MTOR: mechanistic target of rapamycin kinase; OMM: outer mitochondrial membrane; OS: overall survival; PA: phosphatidic acid; PG: phosphatidylglycerol; PGS1: phosphatidylglycerophosphate synthase 1; PINK1: PTEN induced kinase1; PRKAA1/AMPKα1: protein kinase AMP-activated catalytic subunit alpha 1; PRKAA2/AMPKα2: protein kinase AMP-activated catalytic subunit alpha 2; PRKAB1/AMPKβ1: protein kinase AMP-activated catalytic subunit beta 1; PRKAB2/AMPKβ2: protein kinase AMP-activated non-catalytic subunit beta 2; PRKAG1/AMPKγ1: protein kinase AMP-activated non-catalytic subunit gamma 1; PRKN: parkin RBR E3 ubiquitin protein ligase; RCC: renal cell carcinoma; SASA: solvent-accessible surface areas; SUCLG1: succinate-CoA ligase GDP/ADP-forming subunit alpha; TCGA: The Cancer Genome Atlas; TKI: tyrosine kinase inhibitors; UCP1: uncoupling protein 1; ULK1: unc-51 like autophagy activating kinase 1; WCL: whole-cell lysate. - Source: PubMed
Publication date: 2026/02/18
Chen KaileiZhang YuanpengRuan HailongWei ZhihaoWang KeshanCao QiWang QiDong ZiruiWu YilongYang HongmeiLiu LeiLiu YuenanZhang Xiaoping