Ask about this productRelated genes to: CYP2J2 antibody
- Gene:
- CYP2J2 NIH gene
- Name:
- cytochrome P450 family 2 subfamily J member 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-06-21
- Date modifiied:
- 2016-10-05
Related products to: CYP2J2 antibody
Related articles to: CYP2J2 antibody
- CYP2J2 catalyzes the conversion of arachidonic acid into epoxyeicosatrienoic acids (EET), which have gained significant attention due to their oncogenic properties. Differential overexpression of CYP2J2 in tumors results in increased EET production. The role of EET in tumorigenesis is quite clear, but inhibition of CYP2J2 on EET formation with its molecular target is poorly understood. Research is ongoing to identify CYP2J2 inhibitors and the role of the CYP2J2/EET axis in halting tumorigenesis. In these contexts, we aimed to address the same through in silico, in vitro, and in vivo approaches using crocetin, a phyto-based druggable molecule. In vitro mechanistic investigations using human liver microsomes (HLM) indicate that crocetin could act as a specific and reversible CYP2J2 inhibitor. In silico molecular docking analysis and molecular dynamics (MD) simulation explicate strong and stable interactions between crocetin and active site of human CYP2J2. In vivo investigations in BALB/c mice reveal that crocetin could enhance the plasma exposure of rivaroxaban (CYP2J2 substrate) by delaying metabolism and attenuating CYP2J2 protein expression in the liver tissues. Additionally, in vitro studies using HLM and mouse liver microsomes (MLM) suggest that crocetin could substantially hinder EET formation. Thereafter, crocetin showcases its antitumor effect in the mouse model of breast cancer involving downregulation of CYP2J2 expression and impediment of EET formation in the tumor tissues. Further, proteomics data from crocetin-treated tumor tissues with gene ontology analysis (KEGG database) reflect upregulation/downregulation of key proteins and biological processes associated with attenuating tumorigenesis. It is a footstep toward understanding the CYP2J2/EET axis for targeted breast cancer therapy. - Source: PubMed
Publication date: 2026/08/13
Manhas DikshaJamwal AshiyaKaur GursimarAkhter Md QuasidArora NidhiKumar VinayOjha Probir KumarSawant Sanghapal DBag SwarnenduGoswami AnindyaNandi Utpal - Molting disability severely restricts the sustainable aquaculture of the Chinese mitten crab, yet the neuroendocrine mechanisms coordinating physiological responses remain poorly understood. Using unilateral eyestalk ablation to remove the primary source of molt-inhibiting hormone (MIH), we performed time-resolved transcriptomic profiling of the thoracic ganglion at 24 h (early premolt) and 48 h (ecdysis) post-ablation. We identified 2825 differentially expressed genes and uncovered a biphasic molecular response. At 24 h, the thoracic ganglion activates pathways associated with neuromuscular adaptation, oxidative stress, and cardiac muscle contraction. Notably, the arachidonic acid metabolism pathway is selectively rewired: cytochrome P450 ω-hydroxylases (CYP2J2, CYP4V2) are upregulated, while competing branches (epoxide hydrolase, cyclooxygenase) are suppressed, promoting local synthesis of the potent vasoconstrictor 20-HETE within the thoracic ganglion. This enzymatic switch provides a mechanistic link between MIH withdrawal and the local generation of elevated hemolymph pressure required for molting. By 48 h, the transcriptional program shifts toward chitin-based extracellular matrix remodeling, glycosphingolipid biosynthesis, and synaptic reorganization. Collectively, our findings redefine the thoracic ganglion as an active neuroendocrine integrator that translates reduced MIH signaling into phased physiological outputs, revealing a "neuro-endocrine-hemolymph pressure" regulatory axis. This study provides novel molecular targets (e.g., CYP2J2, CHS1, UGCG) for mitigating molting disability in E. sinensis aquaculture. - Source: PubMed
Publication date: 2026/07/30
Fu ChunpengFu XiaopengLi ZongzhenLi FajunWang LifangDong Yunshui - To evaluate associations between polymorphisms in (, ), (), (, ), (, , , ) and () and the occurrence of bleeding or occlusive events in patients receiving rivaroxaban in real-world clinical practice. - Source: PubMed
Publication date: 2026/07/20
Slišković Ana MarijaTrkulja VladimirGanoci LanaBožina TamaraPašara VedranVrkić Kirhmajer MajdaPalić JozefinaStrikić DominikNarančić MarinoSopek Merkaš IvanaMerćep IvetaBulum JoškoŠimičević Livija - Epoxyeicosatrienoic acids (EETs), synthesized by cytochrome P450 epoxygenases (mainly CYP2C9, CYP2J2, and CYP2S1), are vasoprotective lipid mediators that are rapidly degraded by soluble epoxide hydrolase (sEH). This study aimed to examine changes in EET metabolism in T2DM patients with and without DR to understand its potential role in disease pathogenesis and progression. - Source: PubMed
Publication date: 2026/07/13
Sarı İsmailÖzmen EsmaZor Kürşad RamazanErşan SerpilKüçük ErkutAyan DurmuşAbasıkeleş İsmail - This study aimed to investigate the potential molecular mechanisms underlying the therapeutic effects of the traditional Mongolian medicine Zadi-5 on coronary heart disease (CHD). The active compounds of Zadi-5 were identified using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform, and their corresponding targets were retrieved from HERB. The GSE42148 dataset was used to analyze differentially expressed genes (DEGs) associated with CHD. A compound-target network and a disease-gene-target network were constructed, followed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses. Molecular docking was performed to predict binding modes. Furthermore, we employed a CHD model with high-fat diet-fed ApoE mice to explore the protective effects of Zadi-5 in CHD. A total of 250 targets related to the active compounds in Zadi-5 were identified. Additionally, 480 DEGs were screened from the GSE42148 dataset, and seven key targets (MPO, IFNG, TOP2A, PTGS2, CYP2J2, F7, and PPARG) were identified. Molecular docking predicted strong binding affinities between PPARG and the main active components of Zadi-5. Furthermore, Zadi-5 markedly enhanced the heart performance and reduced fibrotic and inflammatory responses in vivo. Zadi-5 effectively suppressed the levels of HIF-1α and increased the PPARG levels in ApoE mice post-myocardial infarction. These findings suggest that the active components of Zadi-5 may exert therapeutic effects in CHD by targeting PPARG, as revealed by network pharmacology and molecular docking analyses. - Source: PubMed
Publication date: 2026/07/07
Xiang JieLiu JingLiu Pengmei