ADRB3
- Known as:
- ADRB3
- Catalog number:
- 001246A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADRB3
Ask about this productRelated genes to: ADRB3
- Gene:
- ADRB3 NIH gene
- Name:
- adrenoceptor beta 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8p11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1993-10-04
- Date modifiied:
- 2015-10-15
Related products to: ADRB3
Related articles to: ADRB3
- Obesity remains a global health challenge, and promoting white adipose tissue browning has emerged as a promising anti-obesity strategy. This study aimed to investigate the anti-obesity effects of denatonium benzoate (DB) and elucidate its underlying mechanisms. - Source: PubMed
Publication date: 2026/04/02
Niu YiqinShao JunhuiTeng YanpingZhang CeXie XinGuo Shimeng - Recent studies have shown that from the 23rd week of gestation onward, the fetus becomes progressively more hypoxic, with oxygenation levels rising again after 33-34 weeks. The biological significance of this biphasic oxygenation pattern has remained unclear. - Source: PubMed
Publication date: 2026/04/03
Scaramuzzo Rosa TeresaFilippini LucreziaCalvani MauraTirinnanzi BiancaCrucitta StefaniaDel Re MarziaMorganti RiccardoDi Marsico LorenzaCammalleri MaurizioBagnoli PaolaDal Monte MassimoPini AlessandroFilippi Luca - - Source: PubMed
Publication date: 2026/03/31
Diani Luísa MariaWatanabe Lígia MoriguchiNoronha Natália Yumida Silva Rodrigues Guilhermede Souza Pinhel Marcela AugustaSae-Lee Chanachaide Oliveira Bruno Affonso ParentiNicoletti Carolina FerreiraJunqueira Gizela PedrosoSalgado WilsonMarchini Júlio SérgioNonino Carla Barbosa - Dihydroquercetin (DHQ) is a promising object for the development of a treatment for patients with obesity and prediabetes requiring a moderate therapeutic effect. This paper reports a clinical case of DHQ application in a 30-year-old Caucasian male and proposes a molecular mechanism of its anti-obesity effect. DHQ was administrated as a dietary supplement at a dose of 100-200 mg/day during 3 months with treatment interruption for 1 month. The data collected one month before the treatment were used as a control. The molecular aspects were studied via molecular docking with β-adrenoceptor (ADRB3, PDB ID: 9IJE) and peroxisome proliferator-activated receptor γ (PPARG, PDB ID: 2ZNO) and molecular dynamic simulation under conditions mimicking a human cellular environment. A pronounced weight decrease up to 0.73 kg/week was observed during DHQ administration. The highest affinity to ADRB3 was observed for the non-ionized H2H3-conformation of 2,3-DHQ (-8.846 kcal/mol). Molecules with 2-configuration demonstrate 0.332 kcal/mol higher affinity to PPARG compared to 2-stereoisomers. The intermolecular complex with -DHQ demonstrated higher stability in molecular dynamics simulation. The insights gained from this study may contribute to our understanding of flavonoids not merely as antioxidants but also as active ingredients that selectively interact with receptors. If future investigations confirm these results, they may serve as a foundation for developing a new class of anti-obesity remedies that act via ADRB3. - Source: PubMed
Publication date: 2026/03/20
Terekhov Roman PTaldaev AmirSvotin Artem APankov Denis ISukhova Evgenia MManukov David ABergel KetelinaKorochkina Maria DSelivanova Irina A - Homeostatic feedback loops are essential to stabilize the activity of neurons and neuronal networks. It has been hypothesized that, in the context of Amyotrophic Lateral Sclerosis (ALS), an excessive gain in feedback loops might hyper- or hypo-excite motoneurons (MNs) and contribute to the pathogenesis. Here, we investigated how the neuromodulation of MN intrinsic properties is homeostatically controlled in presymptomatic adult SOD1(G93A) mice and in the age-matched control WT mice. First, we determined that Adrb2 and Adrb3 adrenergic receptors, which are Gs-coupled receptors and subject to tight and robust feedback loops, are specifically expressed in spinal MNs of both SOD1 and WT mice at P45. We then demonstrated that these receptors elicit a so-far overlooked neuromodulation of the electrical properties of MNs, in particular the frequency-current gain, a crucial determinant of excitability. These electrical properties are homeostatically regulated following receptor engagement, which triggers ion channel transcriptional changes and downregulates those receptors. These homeostatic feedbacks are not dysregulated in presymptomatic SOD1 mice, and they set the MN excitability upon β-adrenergic neuromodulation. - Source: PubMed
Publication date: 2026/03/10
Antonucci StefanoCaron GuillaumeDikwella NatalieKrishnamurthy Sruthi SankariHarster AnthonyWasicki BartoszZarrin HinaTahanis AboudHeuvel Florian OldeDanner Simon MLudolph Albert CGrycz KamilBączyk MarcinZytnicki DanielRoselli Francesco