CYP1A1 EMSA Kit
- Known as:
- CYP1A1 EMSA Kit
- Catalog number:
- AY1290
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- CYP1A1 EMSA Kit
Ask about this productRelated genes to: CYP1A1 EMSA Kit
- Gene:
- CYP1A1 NIH gene
- Name:
- cytochrome P450 family 1 subfamily A member 1
- Previous symbol:
- CYP1
- Synonyms:
- P450DX, P1-450, P450-C, CP11
- Chromosome:
- 15q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
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- Cellular senescence is a core pathogenic mechanism of chronic obstructive pulmonary disease (COPD), and cigarette smoke (CS) acts as its primary risk factor. However, the molecular cascade linking CS exposure to pulmonary cellular senescence remains poorly defined. The aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor triggered by CS-derived chemicals, has an unclarified function in smoke-induced lung cell senescence. This study aimed to verify whether AhR mediates CS-elicited pulmonary senescence through regulating oxidative stress and autophagy, and to elucidate the complete downstream signaling cascade. - Source: PubMed
Publication date: 2026/09/09
Shi Bao-YuHu Xu-DongLiu Yuan-ChengHu Si-MingZhang Guo-Xing - This study employs a multiomics approach to investigate the protective effects of fucoxanthin (Fu) and explore its potential association with metabolic and signaling pathways in diabetic mice induced by a high-fat diet combined with streptozotocin (STZ) administration. Diabetic model mice were randomly divided into normal control (NC), diabetic model, low-dose Fu (50 mg/kg/day), and high-dose Fu (100 mg/kg/day) groups. After 6 weeks of intervention, Fu treatment was associated with dose-dependent improvements in glucose and lipid metabolism, reduced oxidative stress, decreased expression of inflammatory cytokines (tumor necrosis factor-α [TNF-α], interleukin-6 [IL-6], and IL-1β) and renal fibrosis markers (TGF-β1, α-SMA, and Col1a1), along with notable attenuation of renal pathological damage. Exploratory analyses indicated that these phenotypic improvements were accompanied by reduced renal IDO1 expression, favorable shifts in tryptophan (Trp) metabolism, and upregulated AhR/CYP1A1 signaling. 16S rRNA sequencing revealed that Fu treatment was associated with a restoration of diabetes-altered gut microbiota β-diversity. Serum metabolomics identified that Fu administration correlated with alterations in multiple metabolites (including 5'-S-methyl-5'-thioadenosine, LPC 16:0, and bile acids), which are linked to key pathways such as Trp metabolism and bile acid biosynthesis. Network pharmacology predictions further suggested potential multitarget interactions of Fu with the PI3K-Akt and AGE-RAGE signaling pathways. Collectively, these findings indicate that Fu exerts potential renoprotective effects in diabetic mice, which are accompanied by a normalization of Trp-AhR pathway-related metabolism and concurrent attenuation of inflammatory, oxidative, and fibrotic responses. While causal functional links remain to be fully elucidated, these observations provide a preliminary basis for further mechanistic investigation and support the potential of Fu as a dietary supplement or adjunctive strategy for diabetic kidney disease (DKD). - Source: PubMed
Guo DonglinXie JiayongDong XueyunXu HaoXie YunhanLiu XinyuXu LinlinAli AsmaaChen MinZhang LeileiHe JiayuanWu LiangShao Keke - Plasma prorenin is commonly elevated in patients with diabetes and has been associated with the development of albuminuria and progression of diabetic nephropathy. Because albuminuria often reflects podocyte injury, the pathogenic role of prorenin in podocyte dysfunction warrants further investigation. In this study, we examined the association between prorenin and podocyte injury, as well as glomerular fibrosis, using a transgenic rat model in which prorenin is inducibly expressed and secreted from the liver. cyp1a1-prorenin transgenic rats were randomized to receive diets containing increasing concentrations of the gene activator indole-3-carbinol (I3C; 0.05%, 0.15%, or 0.3%) for 4 weeks. Wild-type rats maintained on a normal diet served as controls. I3C administration resulted in a dose-dependent increase in plasma prorenin levels in transgenic rats. Elevated prorenin was associated with increased mean arterial pressure and urinary albumin excretion, accompanied by a dose-dependent reduction in podocyte number and slit diaphragm protein expression, as well as segmental foot process effacement and podocyte hypertrophy. In addition, increased prorenin stimulated renal expression of profibrotic factors and promoted glomerular fibrosis. Treatment with either amlodipine or enalapril for 6 weeks prevented the development of hypertension and partially attenuated podocyte injury, albuminuria, and renal fibrosis, without fully reversing these changes. These protective effects were associated with suppression of NF-κB- and Nox2-mediated inflammatory and oxidative stress pathways. Collectively, these findings demonstrate that prorenin promotes podocyte injury and glomerular fibrosis through mechanisms that are partially dependent on hypertension and angiotensin II but also involve angiotensin II-independent pathways. - Source: PubMed
Publication date: 2026/09/03
Gu ChunyanLiu XiaWu JieHuang Yufeng - Allium sativum L. has a long-standing use in traditional medicine for gastrointestinal disorders. Diallyl sulfide (DAS), a key organosulfur compound derived from garlic, exhibits anti-inflammatory activity; however, its specific role in colitis and the underlying microbiota-metabolite mechanisms remain unresolved. - Source: PubMed
Publication date: 2026/09/12
Wan XiaoyuWu YuanyuSun YananLiu YuxuanJia Guoliang - Benzo[a]pyrene (B[a]P) is a carcinogenic food contaminant formed during thermal processing. Citrus depressa peel, a processing byproduct rich in polymethoxyflavones (PMFs) including nobiletin (NOB), was evaluated for detoxification-related effects in rats. C. depressa peel ethanol extract (CDHPE) was characterized, and its effects on xenobiotic metabolism and B[a]P disposition were assessed. NOB showed measurable oral bioavailability and multi-tissue distribution. Dietary CDHPE or NOB for 7 days increased hepatic phase I/II enzyme activities and intestinal CYP1A1 activity, accompanied by increased hepatic nuclear Nrf2 and reduced ROS levels. Pre-feeding reduced plasma B[a]P AUC by 57-79% and tissue burden by 30-80%, with increased urinary excretion of parent B[a]P. Upregulation of selected Nrf2 downstream target proteins (GCLC, HO-1, NQO1) and significant GCLC mRNA induction are consistent with Nrf2-associated detoxification responses, although causal confirmation by loss-of-function approaches remains needed. These findings support the potential use of citrus peel byproducts as functional ingredients for dietary PAH mitigation. - Source: PubMed
Publication date: 2026/09/04
Li Mei-LingChiang Yu-HsuanHuang Shang-MingYao Hsien-TsungHsu Kuo-Chiang