ADRB1 Antibody
- Known as:
- ADRB1 Antibody
- Catalog number:
- AF1032a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- ADRB1 Antibody
Related genes to: ADRB1 Antibody
- 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 Antibody
Related articles to: ADRB1 Antibody
- Improved access to genetic testing is accelerating identification of variants underlying common sleep traits and rare Mendelian disorders. This review highlights advances over the past two years. - Source: PubMed
Publication date: 2026/09/09
Mani HaritaCuddapah Vishnu Anand - Conotruncal heart defects (CTDs) account for approximately one-third of all congenital heart defects. Elevated levels of phosphatidylinositol (3,4,5)-trisphosphate (PIP3) may contribute to CTD pathogenesis. PIP3 plays a pivotal role in mechanotransduction-based biological processes and remodeling of cardiac cytoskeletal proteins. Here, we aimed to evaluate the efficacy of the 322PESB derivative compound as a molecular regulator that antagonizes PIP3 binding pleckstrin homology (PH) domain of the Akt protein using mesenchymal stem cell-derived cardiomyocyte. Human adipose-derived MSCs (Ad-MSCs) were isolated. Immunophenotypic features of the hAd-MSCs were characterized according to minimal criteria of the international society for cellular therapy (ISCT) including immunophenotyping and trilineage differentiation potential. Subsequently, the differentiated hAd-MSCs were cultured in cardiomyogenesis-inducing medium. Successfully differentiated cardiomyocytes were assessed by measuring the expression levels of cardiomyocyte-specific genes using RT-qPCR. PIP3-primed cardiomyocytes were treated with 10 and 30 μmol/L of a 322PESB derivative molecule. The results showed a typical MSCs with high expression levels of CD73 (77.55%), CD90 (87.59%) and CD105 (91.88%) and that was accompanied by low expression levels of CD34 (0.59%) and CD45 (1.78%). After 21 days of MSC culture, cardiomyocyte-like cells with prominent striations were observed. Subsequent confirmation by RT-qPCR quantification of ADRB1 and MLC2a expression levels showed an average increase of 2.9-fold and 2.1-fold, respectively, in induced cardiomyocytes. Compared with the untreated control, PIP3 ELISA assay showed a significant increase in PIP3 levels in PIP3(10 nmol/L)-primed cardiomyocytes treated with 10 and 30 μmol/L of the 322PESB molecule derivative by 485.804 and 3564.164 ng/mL, respectively. In this study, we conducted the first promising molecular regulator with potential therapeutic implications for CTD patients. Further functional animal model and clinical phase studies are recommended. - Source: PubMed
Publication date: 2026/07/23
Fayez AlaaeldinEsmaiel Nora NRaouf Haiam AbdelAboelenin Mohamad MAly Riham MNour Eldeen Ghada - Nicotine, a major tobacco metabolite and persistent environmental pollutant, is epidemiologically associated with breast cancer risk, yet its non-classical carcinogenic molecular mechanisms and prognostic value remain unclear. This study was designed to systematically elucidate the potential targets and molecular mechanisms underlying the prognostic impact of nicotine on breast cancer, alongside developing an interpretable prognostic risk model. - Source: PubMed
Publication date: 2026/07/21
Weng JunyanOu CaifengYi JiaminYang HuanChen ChiweiHuang Mei - Pharmacogenomics-guided therapy is a promising approach for optimizing antihypertensive treatment response; however, robust real-world data from South Asian and particularly Pakistani populations remain scarce. Understanding genotype-drug response relationships in this underrepresented population is essential to inform context-specific precision prescribing strategies. - Source: PubMed
Publication date: 2026/09/11
Alsubaie NawalIlyas MuhammadShah Zafar AliBinsaleh Ammena YAlrossies Amani SAlmazyad Fahad A - Annexin A4 (A4) is a negative modulator of adenylyl cyclase type 5 (AC5) with increased expression in failing human hearts. Here, we investigated whether A4 deficiency contributes to cardiac electrical and structural remodeling induced by chronic stimulation of β-adrenergic receptors (βAR). A4-deficient mice (gene trapped, GT) and wild-type (WT) were infused for 7 days with isoprenaline (ISO) or NaCl as control. Myocytes of ISO-treated GT (GT) displayed more hypertrophy, increased action potential duration, reduced K-current I, preserved L-type Ca current I with a negative shift of voltage dependence of activation, in line with increased AC/cAMP/PKA signaling, and increased NCX1 versus WT. At the molecular level, mRNA levels for Kcnd3, Kcnip2, Cacna1c decreased at unchanged protein levels of Kv4.2, Kv4.3, KChIP2, α1C, independent of genotype, suggesting posttranslational modifications of the channels underlying I and I. Chronic ISO-induced βAR desensitization and redox stress were confirmed by decreased cAMP production and lower mRNA levels of Adrb1, Adcy5/6, and Sod2, and reduced response to acute ISO, with no additional genotype-dependent effects on calcium handling or contractility. Nevertheless, GT cardiomyocytes retained a greater cAMP response to acute ISO, in line with AC5 disinhibition and preserved β2AR and Gαs/i, suggesting genotype-dependent differences in β-adrenergic signaling under stress. mRNA levels of Anxa4 were increased in hypertrophied WT vs. normal WT hearts, supporting a protective role for A4. Overall, the advanced remodeling in A4-deficient myocytes detected in response to chronic βAR stimulation proposes using A4 peptide as a therapeutic tool to prevent the progression of cardiac electrical remodeling. - Source: PubMed
Pluteanu FlorentinaHeinick AlexanderDomnik-Lehnert ManuelMüller Frank UHermes Christina