GABRQ antibody - N-terminal region (ARP35283_P050)
- Known as:
- GABRQ (anti-) - N-terminal region (ARP35283_P050)
- Catalog number:
- arp35283_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GABRQ antibody - N-terminal region (ARP35283_P050)
Related genes to: GABRQ antibody - N-terminal region (ARP35283_P050)
- Gene:
- GABRQ NIH gene
- Name:
- gamma-aminobutyric acid type A receptor theta subunit
- Previous symbol:
- -
- Synonyms:
- THETA
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 2001-01-24
- Date modifiied:
- 2016-02-04
Related products to: GABRQ antibody - N-terminal region (ARP35283_P050)
Related articles to: GABRQ antibody - N-terminal region (ARP35283_P050)
- Clinical risk factors for seizure presentation in meningioma patients have been reported, but molecular correlates of seizures in meningioma remain unexplored. - Source: PubMed
Publication date: 2026/02/12
Khan A BasitMcDonald Malcolm FEnglish CollinNouri Shervin HKatlowitz Kalman ALau SeanPatel RajanRojas DiegoHarmanci ArifJalali AliRao GaneshPichumani KumarHarmanci Akdes SKlisch Tiemo JPatel Akash J - Growing evidence highlights the critical role of chromatin remodeling in tumor development and progression. This study explores the relationship between chromatin remodeling-related genes (CRRGs) and breast cancer (BRCA). Public databases were used to retrieve the TCGA-BRCA and GSE20685 datasets. CRRGs were sourced from prior studies. Prognosis-associated CRRGs were identified using univariate Cox regression analysis. TCGA-BRCA BRCA samples were grouped into CRRG-related subtypes through consensus clustering analysis. Differential expression analysis was conducted in TCGA-BRCA (BRAC vs. control) and among subtypes to identify differentially expressed genes (DEGs). Candidate genes were obtained through the intersection of these DEGs. Prognostic genes were selected using univariate Cox and least absolute shrinkage and selection operator (LASSO) regression analyses. Independent prognostic factors were identified, and a nomogram model was developed. Functional enrichment, immune infiltration, clinical relevance, and drug sensitivity analyses were subsequently performed. TCGA-BRCA BRCA samples were classified into two CRRG-related subtypes (clusters 1 and 2) based on prognosis-associated CRRGs. A total of 141 candidate genes were identified by intersecting 250 DEGs (cluster 1 vs. cluster 2) with 3,145 DEGs (BRCA vs. control). Five prognostic genes-LHX5, ZP2, GABRQ, APOA2, and CLCNKB-were selected, and a prognostic risk model was developed. In clinical samples, APOA2 (P = 0.0290) and GABRQ (P = 0.0132) expression were significantly up-regulated, CLCNKB (P < 0.0001) and ZP2 (P = 0.0445) expression were significantly down-regulated, while LHX5 (P = 0.1508) expression did not present a significant difference. A nomogram was created, and calibration and Receiver Operating Characteristic (ROC) curves demonstrated its superior predictive ability for BRCA. Gene Set Variation Analysis (GSVA) revealed 16 pathways, such as "mTORC1 signaling" and "E2F targets," were enriched in the high-risk group, while 9 pathways, including "estrogen response early" and "myogenesis," were enriched in the low-risk group. Additionally, significant differences in immune cell types, including CD8 T cells and follicular helper T cells, were observed between the two risk groups. The risk score was also significantly associated with six drugs, including AZD1332 1463 and SB505124 1194. This study presents a prognostic model based on five genes (LHX5, ZP2, GABRQ, APOA2, and CLCNKB) for BRCA, offering a novel perspective on the link between CRRGs and BRCA. - Source: PubMed
Publication date: 2025/05/03
Feng JingChen ZhiqiangWang YuLiu YinghaoZhao DanniGu Xiaodong - As a newly discovered histone modification, abnormal lactation has been found to be present in and contribute to the development of various cancers. The aim of this study was to investigate the potential role between lactylation and the prognosis of breast cancer patients. Lactylation-associated subtypes were obtained by unsupervised consensus clustering analysis. Lactylation-related gene signature (LRS) was constructed by 15 machine learning algorithms, and the relationship between LRS and tumor microenvironment (TME) as well as drug sensitivity was analyzed. In addition, the expression of genes in the LRS in different cells was explored by single-cell analysis and spatial transcriptome. The expression levels of genes in LRS in clinical tissues were verified by RT-PCR. Finally, the potential small-molecule compounds were analyzed by CMap, and the molecular docking model of proteins and small-molecule compounds was constructed. LRS was composed of 6 key genes (SHCBP1, SIM2, VGF, GABRQ, SUSD3, and CLIC6). BC patients in the high LRS group had a poorer prognosis and had a TME that promoted tumor progression. Single-cell analysis and spatial transcriptome revealed differential expression of the key genes in different cells. The results of PCR showed that SHCBP1, SIM2, VGF, GABRQ, and SUSD3 were up-regulated in the cancer tissues, whereas CLIC6 was down-regulated in the cancer tissues. Arachidonyltrifluoromethane, AH-6809, W-13, and clofibrate can be used as potential target drugs for SHCBP1, VGF, GABRQ, and SUSD3, respectively. The gene signature we constructed can well predict the prognosis as well as the treatment response of BC patients. In addition, our predicted small-molecule complexes provide an important reference for personalized treatment of breast cancer patients. - Source: PubMed
Publication date: 2025/04/19
Zhao JinfengLi LongpengWang YaxinHuo JiayuWang JiruiXue HuiwenCai Yue - Fabry disease (FD) is a rare X-linked lysosomal storage disorder caused by a deficiency in the enzyme α-galactosidase A. This defect leads to the progressive accumulation of glycosphingolipids, resulting in kidney, heart, and nervous system damage, which contributes to significant morbidity and mortality. Early diagnosis is essential to prevent irreversible damage and optimize treatment strategies. Recent research aims to provide a better understanding of FD pathophysiology to improve management approaches. This study is an international, multicenter, cross-sectional analysis that used RNA sequencing (RNA-seq) to compare blood samples from 50 FD patients and 50 age- and sex-matched healthy controls. The objective was to identify gene expression patterns and investigate secondary cellular pathways affected by lysosomal dysfunction. Among the more than 400 differentially expressed genes detected, 207 were protein-coding genes, most of which were overexpressed in the FD cohort. Functional enrichment analysis highlighted processes related to synaptic function, specifically concerning chemical synaptic transmission and membrane potential regulation. Identified genes included those related to voltage-gated ion channels, neurotransmitter receptors, cell adhesion molecules, scaffold proteins, and proteins associated with synaptic vesicles and neurotrophic signaling, all linked to lipid rafts. Notable identified genes included those encoding voltage-gated potassium channel genes (KCNQ2, KCNQ3, KCNMA1) and ionotropic receptor genes involved in glutamatergic (GRIN2A, GRIN2B) and GABAergic systems (GABRA4, GABRB1, GABRG2, GABRQ). These findings suggest that lysosomal dysfunction contributes to synaptic defects in FD, paving the way for further research into the role of synaptic pathology and lipid rafts in the underlying pathogenesis and clinical outcomes in FD. - Source: PubMed
Publication date: 2025/04/13
López-Valverde LauraVázquez-Mosquera María EColón-Mejeras CristóbalÁlvarez J VíctorLópez-Pardo Beatriz MartínLópez Lluis LisSánchez-Martínez RosarioLópez-Mendoza ManuelLópez-Rodríguez MónicaVillacorta-Argüelles EduardoGoicoechea-Diezhandino María AGuerrero-Márquez Francisco JOrtolano SaidaLeao-Teles ElisaHermida-Ameijeiras ÁlvaroCouce María L - To explore the therapeutic effects and underlying mechanisms of Dendrobium officinale (Tiepi Shihu) extract (DOE) on insomnia. - Source: PubMed
Publication date: 2025/04/15
Zhou Heng-PuSu JieWei Ke-JianWu Su-XiangYu Jing-JingYu Yi-KangNiu Zhuang-WeiJin Xiao-HuYan Mei-QiuChen Su-HongLyu Gui-Yuan