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 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 - Breast cancer is a very common disease affecting females on a global scale. It is responsible for approximately 10% of breast cancer-related fatalities. In 2022, approximately 2,308,897 new cases were reported globally. Recent studies focused on breast tumors have successfully recognized somatic mutations. This study aimed to identify previously unidentified somatic mutations in breast cancer patients belonging to Pakistan. - Source: PubMed
Publication date: 2025/07/31
Nawaz YasirMunir SabaTanvir FouziaRiaz Hafiza FizzahNawaz AqeelaRiaz Samreen - Colorectal cancer (CRC) and type 2 diabetes mellitus (T2DM) exhibit interrelated pathologies, yet the underlying mechanisms of their interaction remain largely elusive. GeGen-QinLian decoction (GQD) has shown therapeutic efficacy in both CRC and T2DM. This study aimed to elucidate the potential pharmacological mechanisms of GQD in the postoperative treatment of patients with CRC and T2DM. Transcriptomic data sets for CRC and T2DM were retrieved from The Cancer Genome Atlas and Gene Expression Omnibus databases. Differential expression analysis, univariate Cox regression analysis, and weighted gene coexpression network analysis were employed to identify shared genes between CRC and T2DM. Network pharmacology was used to analyze the bioactive components of GQD and their targets, identifying potential therapeutic targets for the concurrent treatment of T2DM and CRC. Enrichment analysis, immune infiltration assessment, and drug sensitivity analysis were performed, complemented by molecular docking to validate the affinity between potential targets and active components. A total of 433 shared genes between CRC and T2DM were identified, involving processes such as gene expression regulation, cell cycle control, apoptosis regulation, Wnt signaling pathway, regulation of NF-κB transcription factor activity, and inflammatory mediator regulation of transient receptor potential channels. We identified 204 bioactive components of GQD and 320 corresponding targets, of which 10 (ADRA1B [adrenergic receptor alpha 1B], CALM1 [calmodulin 1], CDKN2A [cyclin-dependent kinase inhibitor 2A], CTNNA1 [cadherin-associated protein], FCER2 [Fc fragment of IgE receptor II], GSR [glutathione reductase], GSTM1 [glutathione S-transferase mu 1], IL13 [interleukin 13], INSR [insulin receptor], and MAPK9 [mitogen-activated protein kinase 9]) were determined as potential targets for the treatment of T2DM and CRC using GQD. Enrichment analysis revealed that these targets were associated with pathways including insulin signaling pathway, cyclic guanosine monophosphate-protein kinase G signaling pathway, Ras signaling pathway, and Fc-epsilon receptor I signaling pathway. Molecular docking results demonstrated high affinity between these potential targets and active components, with the highest affinity observed between CALM1 and xambioona. This study systematically identified a set of shared genes between T2DM and CRC, along with the bioactive components and 10 potential targets of GQD for the treatment of T2DM and CRC. These findings provided a theoretical foundation for the combined therapy of T2DM and CRC. - Source: PubMed
Liang JinhaoXiang ChengjiangLiang Yuanxiao