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  • mProX™ Human ADRA1B Stable Cell Line

    [CAT#: S01YF-0923-PY6]
    Product Category:
    Membrane Protein Stable Cell Lines
    Subcategory:
    GPCR Cell Lines

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    Product Information

    Target Protein
    ADRA1B
    Target Family
    Adrenergic Family
    Target Protein Species
    Human
    Host Cell Type
    THP-1;CHO-K1;HEK293
    Target Classification
    GPCR Cell Lines
    Target Research Area
    Cancer Research
    Related Diseases
    Prostatic Hypertrophy
    Gene ID
    Human: 147
    UniProt ID
    Human: P35368

    Product Properties

    Biosafety Level
    Level 1
    Activity
    Yes
    Quantity
    10⁶ cells per vial
    Applications
    Adrenergic α1B receptor (ADRA1B) has been identified as a significant receptor in scientific research, especially in relation to neurotransmission and cardiovascular health. One of the intriguing findings is the functional coupling between GPR143, an L-DOPA receptor, and ADRA1B. This interaction augments the ADRA1B-mediated response, suggesting that L-DOPA itself might act as a neurotransmitter. Additionally, certain gene variants of ADRA1B have been associated with psoriasis susceptibility in the Chinese population, indicating its potential role in immune-mediated skin disorders. Furthermore, ADRA1B has been implicated in the vasodilation of lung vessels, especially in response to the diving reflex. These findings highlight the diverse roles of ADRA1B in various physiological and pathological processes, emphasizing its significance in scientific research and potential therapeutic applications.

    Protocols

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    FAQ

    chat William (Verified Customer)

    How do alpha-1 adrenergic antagonists influence neuroblastoma cells? May 26 2023

    chat Patrick Liam (Creative Biolabs Scientific Support)

    Alpha-1 adrenergic antagonists can sensitize neuroblastoma cells to therapeutic differentiation, with the α1B adrenergic receptor identified as a potential pharmacological target. May 26 2023

    chat Melissa (Verified Customer)

    Are there any known associations between ADRA1B and blood pressure regulation? Sep 01 2021

    chat Patrick Liam (Creative Biolabs Scientific Support)

    While ADRA1B plays a role in adrenergic signaling, specific gene polymorphisms like ADRB3 T727C are more directly linked to the antihypertensive effects of certain medications. Sep 01 2021

    Published Data

    Fig.1 The migration of control and THP-1-ADRA1B-KO cells toward various CR agonists.

    THP-1-ADRA1B-KO cells' chemotactic responses mediated by CCR1, CCR2, and CXCR4 were reduced by 95, 82, and 91%, respectively, when compared to control cells. THP-1-ADRA1BKO and wild-type control cells migrated indistinguishably toward the CCR8 agonist. These findings show that the presence of 1B/D-ARs is required for CR heteromerization partners to migrate toward their chemokine agonists.

    Ref: Enten, Garrett A., et al. "α1B/D-adrenoceptors regulate chemokine receptor-mediated leukocyte migration via formation of heteromeric receptor complexes." Proceedings of the National Academy of Sciences 119.20 (2022): e2123511119.

    Pubmed: 35537053

    DOI: 10.1073/pnas.2123511119

    Research Highlights

    Carnes MU, et al. "Smoking-informed methylation and expression QTLs in human brain and ." medRxiv : the preprint server for health sciences, 2023.
    Smoking is a major cause of preventable morbidity and mortality. Recent studies have shown that smoking has a heritable component, and genome-wide association studies (GWAS) have identified numerous significant loci related to smoking behaviors. A team of researchers utilized genome-wide genotype, DNA methylation, and RNA sequencing data from postmortem human nucleus accumbens (NAc) to identify methylation/expression quantitative trait loci (meQTLs/eQTLs), explore interactions between genetic variants and smoking, and evaluate the regulatory potential of smoking GWAS-identified loci. The study included 52 active smokers and 171 nonsmokers, and used a two-stage multiple testing approach to analyze the data. The results showed over 2 million significant meQTL variants and 57,683 significant eQTLs. Additionally, five meQTLs showed a significant interaction with smoking. Colocalization analyses revealed that certain GWAS-identified loci associated with smoking overlapped with meQTLs/eQTLs, suggesting that these genetic factors may influence smoking behaviors through effects on methylation and expression. Particularly, the locus containing MUSTIN1 and ITIH4 showed overlap across all data types. This study is the first to provide a genome-wide map of meQTLs in the human NAc, and the overlap with smoking GWAS-identified loci suggests that gene regulation in the brain may play a role in the neurobiology of smoking behaviors.
    Pubmed: 37790540   DOI: 10.1101/2023.09.18.23295431

    Yang C, et al. "Human dental pulp stem cells are subjected to metabolic reprogramming and ." Journal of endodontics, 2023.
    The effects and underlying mechanisms of the sympathetic nervous system (SNS) on human dental pulp stem cells (hDPSCs) have remained elusive. To address this, a study was conducted to investigate the effects of the SNS on the proliferation and migration of hDPSCs. The distribution of sympathetic nerve fibers in human dental pulp was examined using immunofluorescence staining, and norepinephrine (NE) levels were measured via ELISA in both healthy and carious pulp tissues. Additionally, RNA-sequencing was performed to identify the dominant sympathetic neurotransmitter receptor in hDPSCs. This study revealed the inhibitory effects of the SNS on hDPSC proliferation and migration, and demonstrated that this is mediated through metabolic reprogramming via the adrenergic receptor alpha 1B (ADRA1B) and its interaction with AKT and p38 MAPK signaling pathways. These findings highlight the important role of the SNS in maintaining the quiescent state of hDPSCs.
    Pubmed: 37769871   DOI: 10.1016/j.joen.2023.09.007

    Please note: All products are "FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC OR CLINICAL PROCEDURES" For licensing inquiries, please contact
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