eNOS (Phospho-Thr494) Antibody
- Known as:
- eNOS (Phospho-Thr494) Antibody
- Catalog number:
- 11711
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- eNOS (Phospho-Thr494) Antibody
Related genes to: eNOS (Phospho-Thr494) Antibody
- Gene:
- NOS3 NIH gene
- Name:
- nitric oxide synthase 3
- Previous symbol:
- -
- Synonyms:
- ECNOS, eNOS
- Chromosome:
- 7q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-08-23
- Date modifiied:
- 2016-10-05
Related products to: eNOS (Phospho-Thr494) Antibody
Related articles to: eNOS (Phospho-Thr494) Antibody
- Cerebral ischemia/reperfusion injury (CIRI) is a major cause of neurological dysfunction after ischemic stroke, and effective therapies remain limited. Gomisin A, a bioactive lignan isolated from Schisandra chinensis, exhibits antioxidant and anti-apoptotic activities, but its role in CIRI remains unclear. Here, the protective effects of Gomisin A were investigated using middle cerebral artery occlusion (MCAO) rats and oxygen-glucose deprivation/reoxygenation (OGD/R) cell models. Gomisin A significantly reduced cerebral infarct volume and improved neurological outcomes in MCAO rats. In OGD/R models, it enhanced endothelial cell migration and tube formation, accompanied by increased VEGF expression and activation of the VEGF/PI3K/AKT/NOS3 signaling pathway. In addition, Gomisin A alleviated oxidative stress and suppressed apoptosis in both cellular and animal models. Pharmacological inhibition of VEGF with axitinib partially reversed these protective effects, supporting the involvement of VEGF-dependent signaling. Collectively, these findings suggest that Gomisin A exerts neuroprotective effects against CIRI by enhancing angiogenic activity while attenuating oxidative stress and apoptosis, partly through activation of the VEGF/PI3K/AKT/NOS3 pathway. Gomisin A may therefore represent a promising candidate for the treatment of ischemic stroke. - Source: PubMed
Publication date: 2026/08/14
Zhao ChengheYu JiayueLiu KexinWang ShuanglingJing WenpingZhao ZiyiZhuang Wenyue - - Source: PubMed
Zakirova GulnozaMasharipova DilyafruzBoboev QodirjonTagaeva Dilnoza - - Source: PubMed
Jabbar AlishbaFatima MinahilGul SalehaNoor Kashaf - Aberrant DNA methylation is a hallmark of acute myeloid leukemia (AML) and contributes to leukemogenesis, treatment response, and clinical heterogeneity. While genome-wide methylation studies have identified prognostic methylation signatures, the impact of DNA methylation within pharmacologic pathways and AML-relevant disease genes remains incompletely understood. We investigated the association of DNA methylation in genes of pharmacokinetic/pharmacodynamic (PK/PD) pathways of drugs used to treat AML and in myeloid leukemia-related genes with treatment outcomes in pediatric AML. - Source: PubMed
Publication date: 2026/07/31
Alshameri NaifahMarchi FranciscoCao XueyuanRubnitz Jeffrey ERibeiro Raul CMeshinchi SoheilPounds Stanley BLamba Jatinder K - Despite advances in therapy, arterial, venous, and pulmonary vascular diseases remain leading causes of morbidity and mortality. Persistent endothelial dysfunction, inflammation, oxidative stress, and maladaptive vascular remodeling continue to drive disease progression and residual risk. CRISPR/Cas9 technology offers a unique opportunity to modify the molecular pathways underlying vascular pathophysiology directly. The PRISMA 2020 guidelines guided the systematic review. The databases PubMed/MEDLINE, Embase, Web of Science, Cochrane Library, ClinicalTrials.gov, and Google Scholar were searched from their inception until September 2025 for experimental and/or clinical studies evaluating the application of CRISPR/Cas9 on vascular disease. Included were in vitro studies, animal model studies, and early-phase human studies aimed at targeting the endothelial cell regulatory pathways, inflammatory pathways, metabolic remodeling processes, and hereditary causes of vasculopathy. Seventeen studies met the inclusion criteria. CRISPR technologies targeting PCSK9, NOS3, HIF1A, NLRP3, METTL4, BMPR2, and ACTA2 were identified to enhance repair mechanisms in endothelial cells, regulate inflammation, modulate lipid metabolism, and remodel the vascular system. The human studies demonstrated sustained gene silencing effects following a single dose of CRISPR-induced in vivo editing. The use of CRISPR technology to edit cell genomes offers potential to alter disease progression in vascular medicine, with a growing body of translational evidence supporting the feasibility and durability of the approach. - Source: PubMed
Publication date: 2026/08/08
Ahad AbiyaHullon DarshanSingh TanyaDabiry Sultan MujibSakthivel LalenthikaPadaria JeelRekhraj Akshay SinghBhattacharjee Aditya