Ask about this productRelated genes to: ADRA1B Blocking Peptide
- Gene:
- ADRA1B NIH gene
- Name:
- adrenoceptor alpha 1B
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 5q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-06-04
- Date modifiied:
- 2019-03-22
Related products to: ADRA1B Blocking Peptide
Related articles to: ADRA1B Blocking Peptide
- The -adrenergic receptor, encoded by , couples to heterotrimeric G proteins, promoting intracellular calcium mobilization and PKC activation. In human hepatocytes, it regulates acute metabolic responses and impacts gene expression. Although fundamental hepatic functions of have been described, its role in hepatocellular carcinoma remains elusive. We hypothesized that expressed in liver cancer tissue is part of a signaling repertoire potentially linked to patient outcomes. We analyzed The Cancer Genome Atlas liver cancer datasets and found gene deletion in 6% of patients and more prolonged survival of patients with high expression. Thus, we aimed to identify -signaling partners equally linked to more prolonged patient survival. Through a rational data mining strategy, based on the identification of the signaling repertoire linked to expression and statistical correlation with patient survival, we identified a transcriptional signature integrated by the adrenoceptor and five candidate signaling companions including two RhoGEFs: and , a phospholipid phosphatase: , a RabGAP: , and an RTK adaptor: . Additionally, highly co-expressed GPCRs such as , , , , , and , and RTKs like and similarly integrated transcriptional signatures with that correlated with more prolonged survival. Most candidate signaling partners were well-co-expressed with hepatocyte markers, suggesting that integrating -associated signaling networks could improve liver cancer patients' prognosis. - Source: PubMed
Publication date: 2026/07/31
Beltrán-Navarro Yarely MabellVázquez-Prado JoséReyes-Cruz GuadalupeGarcía-Sáinz Jesús Adolfo - Neuroticism is an established risk factor for Alzheimer's disease (AD), yet the molecular mechanisms linking this personality trait to neurodegeneration remain poorly understood. - Source: PubMed
Publication date: 2026/06/29
Sharma SnehaComandante-Lou NatachaMa YiyiFujita MasashiBennett David AZammit Andrea RDe Jager Philip L - The brain regulates liver metabolism through neuroendocrine and autonomic pathways, which can be disrupted in metabolic dysfunction-associated steatotic liver disease (MASLD). Although autonomic dysfunction, including liver neuropathy, has been reported in MASLD, the role of hepatic sympathetic signaling in disease progression remains unclear. Recent studies show that liver innervation is predominantly of a sympathetic nature, suggesting that adrenergic receptors in hepatocytes may influence the pathogenesis of MASLD. We previously identified adrenoceptor alpha-1b (ADRA1B) as the dominant hepatic adrenergic receptor. Here, we hypothesized that ADRA1B plays a protective role in MASLD progression. To test this, we generated hepatocyte-specific knockout mice () and induced MASLD with the Gubra Amylin NASH diet for up to 32 wk. Liver pathology was quantified by automated image analysis (MorphoQuant), and metabolic phenotyping included glucose tolerance, insulin sensitivity, and bile acid composition. Hepatocyte-specific deletion did not affect body weight, hepatic lipid accumulation, glucose tolerance, or insulin sensitivity. However, mice exhibited significantly increased hepatic inflammation compared to wild-type controls. These changes were associated with higher hepatic expression of tumor necrosis factor () and interleukin-1b (), as well as an increase in monocyte chemoattractant protein-1 (MCP-1) and interleukin-6 (IL-6). We also observed elevated transforming growth factor beta (TGF-β) and α-smooth muscle actin () expression, suggesting activation of hepatic stellate cells. In addition, mice displayed higher circulating bilirubin levels, with no significant alterations in albumin and bile acid pool composition. These findings reveal a previously unrecognized role for hepatic ADRA1B in restraining inflammatory responses in MASLD. Loss of signaling promotes hepatic inflammation, highlighting a neuroimmune mechanism that may be targeted to prevent disease progression. This study identifies the hepatic α1b adrenoceptor (ADRA1B) as a regulator of inflammation in metabolic dysfunction-associated steatotic liver disease (MASLD). Using a hepatocyte-specific knockout model, we show that loss of exacerbates hepatic inflammatory responses without affecting steatosis or systemic metabolism. These findings reveal a previously unknown immune mechanism in liver disease progression. - Source: PubMed
Publication date: 2025/10/14
Efole BernieBeji SarraMouchiroud MathildeGélinas YvesCanivet CoralineTrottier JocelynSerdjebi CindyElmquist Joel KDeslauriers JessicaBarbier OlivierCaron Alexandre - Maternal childhood maltreatment (CM) has been associated with subsequent difficult infant temperament. Further, maternal CM and maladaptive infant outcomes have each been linked, separately, to increased methylation in umbilical cord blood of CpG sites in genes related to the stress response and inflammatory markers. Researchers have not yet examined the nature of the interactions of these factors or whether DNA methylation (DNAm) mediates or moderates the association of maternal CM with infant temperament. - Source: PubMed
Publication date: 2025/09/19
Parks Kendall CButhmann Jessica LTeh Ai LingChen LiChen Helen YGotlib Ian H - We reported previously that α-AR (α-adrenoceptor) and AVPR1A (arginine vasopressin receptor 1A) heteromerize with CCR1 (C-C motif [chemokine] receptor 1) in human monocytes, through which CCR1 is controlled. Whether CCR1 affects α-AR and AVPR1A signaling and whether such complexes are detectable in human vascular smooth muscle cells (hVSMCs) is unknown. - Source: PubMed
Publication date: 2025/08/18
Gao XianlongCook Elizabeth ABoshra Sadia NOgunsina Ololade RMajetschak Matthias