CHRNB2 antibody - middle region (ARP37669_T100)
- Known as:
- CHRNB2 (anti-) - middle region (ARP37669_T100)
- Catalog number:
- arp37669_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CHRNB2 antibody - middle region (ARP37669_T100)
Related genes to: CHRNB2 antibody - middle region (ARP37669_T100)
- Gene:
- CHRNB2 NIH gene
- Name:
- cholinergic receptor nicotinic beta 2 subunit
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-05-11
- Date modifiied:
- 2016-02-04
Related products to: CHRNB2 antibody - middle region (ARP37669_T100)
Related articles to: CHRNB2 antibody - middle region (ARP37669_T100)
- Nasopharyngeal carcinoma (NPC) is a malignant tumor of the nasopharyngeal mucosal epithelium. The aryl hydrocarbon receptor (AhR)-a widely distributed nuclear receptor regulating adaptive adverse responses-is confirmed carcinogenic upon activation. Thus, this study aims to identify novel biomarkers for NPC treatment. - Source: PubMed
Publication date: 2026/07/27
Liang QiulinCao ChangxingZou ZilingPeng YulanFeng Chao - Beige-adipocyte activity, mediated by CHRNA2, significantly influences adipose function and systemic metabolism. The CHRNB2 subunit forms a functional receptor with CHRNA2 and is essential for the response to nicotinic acetylcholine receptor agonists in beige adipocytes. Deletion of Chrnb2 in mice compromises the adaptive response to cold in subcutaneous adipose tissue and renders exacerbated metabolic dysfunction due to diet-induced obesity. This cholinergic signaling within subcutaneous adipose tissue declines with aging. CHRNB2 partial agonists, a family of drugs clinically used for smoking cessation, activate both murine and human beige adipocytes. - Source: PubMed
Publication date: 2026/05/13
Liu ShanshanZhu KezhouZhang WenwenPan TongO'Brien MartinAbe IchitaroDale LilyPiejak JustinHoussein NadiaZhang BiyangFein MatthewKajimura ShingoYung RaymondXu X Z ShawnWu Jun - Schizophrenia (SCZ) is a highly heritable neuropsychiatric disorder. Its genomic architecture reportedly overlaps with that of neurodevelopmental disorders, such as attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). However, the effect of genomic risk for ADHD and ASD on SCZ symptoms remains unclear. - Source: PubMed
Publication date: 2026/04/27
Miyahara KazusaHino MizukiShishido RisaNagaoka AtsukoHamasaki HideomiKakita AkiyoshiTomita HiroakiKunii Yasuto - Lidocaine, a widely used local anesthetic, has been reported to exert anti-cancer activity against hepatocellular carcinoma (HCC). However, its molecular mechanisms remain incompletely understood. This study sought to elucidate the mechanisms underlying lidocaine’s effects on HCC. Potential lidocaine targets in HepG2 cells were identified using network pharmacology and transcriptomic profiling. The prognostic and clinical relevance of candidate genes were assessed through bioinformatics analyses. Key targets were validated by RT–qPCR. The functional role of SLC6A3 in regulating HepG2 cell proliferation, apoptosis, migration, and invasion was examined through in vitro assays. Network pharmacology predicted 433 lidocaine targets, while transcriptomic profiling revealed 442 differentially expressed genes. Nine overlapping targets (SLC6A3, CHRNB2, GRIN1, ADRA2C, LIPE, SLC18A2, KCNQ2, TERT, and ALOX12) were enriched in pathways associated with neuronal signaling, synaptic transmission, and drug addiction. Among these, SLC6A3 and TERT were significantly associated with poor prognosis and increased tumor immune infiltration. Both genes demonstrated predictive value for 1- to 2-year survival, with SLC6A3 showing the stronger prognostic relevance. Molecular docking revealed hydrophobic interactions between lidocaine and SLC6A3 (binding energy: −5.6 kcal/mol). Silencing of SLC6A3 markedly promoted apoptosis and suppressed proliferation, migration, and invasion of HepG2 cells. Collectively, these findings suggest that lidocaine inhibits HCC progression by targeting and downregulating SLC6A3. Lidocaine exerts anti-HCC effects by directly targeting and downregulating SLC6A3, thereby inducing apoptosis and suppressing tumor progression. - Source: PubMed
Publication date: 2026/04/07
Li PeiyangTong WulanHe HongLiu HaoYang Xi - Lateral temporal lobe epilepsy (LTLE) is characterized by auditory auras and is often associated with genetic factors. Previous studies have identified various genes linked to LTLE, including . However, there remains a need to explore other genetic variants that contribute to the LTLE phenotype, particularly in the absence of mutations. - Source: PubMed
Publication date: 2026/02/19
Salman BarışKesim YeşimŞirin Nermin GörkemSüsgün SedaUzun Güneş Altıokkaİşeri Sibel UğurBebek NersesBaykan Betül