Ask about this productRelated genes to: ADRB1 Blocking Peptide
- Gene:
- ADRB1 NIH gene
- Name:
- adrenoceptor beta 1
- Previous symbol:
- ADRB1R
- Synonyms:
- -
- Chromosome:
- 10q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2015-08-24
Related products to: ADRB1 Blocking Peptide
Related articles to: ADRB1 Blocking Peptide
- Lung cancer, LUAD, and LUSC are both among the leading causes of cancer-related deaths. T cell exhaustion within the tumor microenvironment compromises the immune response and limits the benefits of immune checkpoint therapy. Adrenergic signaling primarily through ADRB1 induces T cell exhaustion and immune suppression. ADRB1 + T cells have not yet been studied regarding their role in lung cancer progression or prognosis. scRNA-seq analysis for tumor and adjacent nontumor tissues from patients with LUAD and LUSC. Dimensionality reduction and clustering with Scanpy, followed by ssGSEA for adrenergic signaling activity. CNV was processed with inferCNV, and cell-to-cell communication was inferred via CellChat. Integration with TCGA bulk RNA-seq data enables prognostic modeling of ADRB1 T cells. Kaplan-Meier survival analysis and univariate Cox regression were used to study the signature of ADRB1 + T cells for prognostic value. - Source: PubMed
Publication date: 2026/04/29
Cao ZhanqiSu FanDun XinjieLu QianchengXu HaoranSu PengyangXue ZhongkaiWang ShiboYang XiuzhiXu Hanlin - Stress is known to play a critical role in relapse to drug use as well as in food craving. Craving itself is a key determinant of relapse, and cue-induced drug craving has been shown to increase, or 'incubate', over time for certain drugs such as cocaine and nicotine, though this effect is less consistent for others such as opiates. However, the modulations of stress-related biochemical systems after early or protracted withdrawal that could contribute to this incubation phenomenon have not yet been systematically examined in animal models, nor has the specificity of these mechanisms been tested across different drug classes or reinforcers. To address this gap, we analysed brains from male Lewis rats that self-administered cocaine (0.75 mg/kg, i.v.), heroin (0.075 mg/kg, i.v.), or saline, and subsequently assessed changes in plasma corticosterone, ornithine and other stress-related amines, alongside central gene and protein expression CRH, CRH2 receptor, and α- and β-adrenergic receptor subunits -Adra1, Adra2a and Adrb1) in cortico-striato-amygdalar nodes (after 1 or 30 days of withdrawal). A parallel experiment was conducted using sucrose as a reinforcer. Our findings indicate that although most effects were reinforcer-specific, convergent adaptations were also observed, particularly within noradrenergic systems and the basolateral amygdala, expanding our knowledge about the neurochemical rearrangements occurring during withdrawal. - Source: PubMed
Publication date: 2026/04/16
Roura-Martínez DavidUcha MarcosMoreno-Fernández MarioCastillo Carlos AlbertoBallesteros-Yáñez InmaculadaMarcos AlbertoAmbrosio EmilioHiguera-Matas Alejandro - Antihypertensive therapy is pivotal in preventing cardiovascular events, yet treatment efficacy varies significantly among individuals due to genetic polymorphisms.This study aimed to investigate the association between specific antihypertensive drug-related gene polymorphisms, the use of corresponding sensitive drugs, and the risks of stroke and coronary heart disease (CHD) in a community-based hypertensive population. A cross-sectional study was conducted among 29,662 hypertensive patients from primary care centers in Changsha County, China. Seven gene loci (ACE(I/D), CYP2C9*3,AGTR1(1166 A > C), CYP2D6*10,ADRB1(1165G > C), CYP3A5*3, and NPPA(2238T > C))were genotyped.Patients were stratified into sensitive or non-sensitive genotype groups. Logistic regression and interaction analysis were employed to assess gene-drug interactions on cardiovascular outcomes. The prevalence of stroke and CHD was 2.8% and 19.5%, respectively. Carriers of sensitive genotypes for AGTR1, CYP2D6*10, and ADRB1 taking sensitive drugs exhibited a significantly lower risk of stroke (ORs: 0.39, 0.67, 0.68; all P < 0.01). Similarly, sensitive genotype carriers for CYP2D6*10, CYP3A5*3, and NPPA taking sensitive drugs had a reduced risk of CHD (ORs: 0.92, 0.88, 0.53; all P < 0.05). A significant additive interaction was identified between AGTR1(1166 A > C) and sensitive drug use on CHD risk (AP = 0.08). Pharmacogenomics-guided antihypertensive therapy is associated with a reduced risk of stroke and CHD in hypertensive patients. The interaction between AGTR1(1166 A > C) genotype and drug use underscores the potential of personalized medicine in optimizing cardiovascular disease prevention strategies in primary care. - Source: PubMed
Publication date: 2026/04/12
Li ZetongLiu HuixiaChen MengshiDeng JingMa ZiyuHuang GeLi ChengSu MengZhong Hua - Understanding the molecular mechanisms underlying mycotoxin toxicity is crucial for risk assessment and public health protection. In this study, we performed comprehensive molecular docking analysis of 434 structurally diverse mycotoxins against a panel of 44 human protein targets associated with acute toxicity effects. Docking results revealed that 18.2% of all interactions had binding energies ≤ -9 kcal/mol. We identified which proteins across the panel were most vulnerable to mycotoxins: acetylcholinesterase, serotonin transporter, and adrenergic receptors (ADRB1 and ADRB2). Analysis identified most promiscuous mycotoxins, including β-asperlicin C and ergotamine, the latter demonstrating the most favorable predicted binding to HTR1B ([Formula: see text] kcal/mol), consistent with experimental data. Class-specific binding pattern analysis revealed that aflatoxins and ochratoxins exhibit broad multi-target activity. These findings provide systematic insights into the molecular basis of mycotoxin toxicity and identify priority targets for future experimental validation and public health monitoring strategies. The dataset containing the affinity data is publicly available at https://github.com/chemagents/mycotoxins-antitargets. - Source: PubMed
Publication date: 2026/04/06
Tkachenko VarvaraNikitin IliaMorgunov IgorSafronov VictorLeleytner AdeliyaKalyuzhnaya AnnaFedorov Maxim - Preeclampsia is a leading cause of maternal and perinatal morbidity and mortality, and a major contributor to low birth weight. Beta blockers (BB) and calcium channel blockers (CCB) are the most commonly recommended agents to treat hypertension in pregnancy. Yet it remains unknown whether these agents alter the risk of preeclampsia (PE), and if so, whether effects arise through maternal physiology or through direct fetal mechanisms. - Source: PubMed
Publication date: 2026/03/23
Ardissino MaddalenaMorley Alec PRichards Eleanor M FZöllner JuliaTruong BuuWilliamson CatherineHonigberg Michael CWare James SNicolaides Kyprosde Marvao Antonio