GNAZ Antibody
- Known as:
- GNAZ Antibody
- Catalog number:
- abx000778
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- GNAZ Antibody
Related genes to: GNAZ Antibody
- Gene:
- GNAZ NIH gene
- Name:
- G protein subunit alpha z
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 22q11.22-q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1989-03-07
- Date modifiied:
- 2018-02-13
Related products to: GNAZ Antibody
Related articles to: GNAZ Antibody
- Vasculogenic mimicry (VM) is a microcirculation pattern that has a crucial effect on hepatocellular carcinoma (HCC) metastasis. In this study, leveraging the GeneCard and The Cancer Genome Atlas databases, we identified ATPase inhibitory factor 1 (IF1) as a potential regulator of VM formation. Our research findings indicate that IF1 can promote HCC cell tube formation in vitro and enhance HCC VM and lung metastasis in vivo. Transcriptome sequencing combined with in vivo experiments revealed that IF1 knockdown elevates miR-20a-3p expression. Lentivirus-mediated miR-20a-3p overexpression reversed IF1-induced VM. Dual-luciferase reporter gene assays showed that estrogen receptor 1 (ESR1) acts as a transcription factor of the miR-20a-3p precursor. Further mechanistic studies revealed that excessive reactive oxygen species accumulation caused by IF1-induced mitochondrial metabolic reprogramming can inhibit ESR1 expression by promoting DNA methylation of its promoter. G protein subunit alpha Z (GNAZ), a miR-20a-3p target protein, can promote VM by phosphorylating components of the ERK pathway. Collectively, these results delineate a novel IF1/ESR1/miR-20a-3p/GNAZ axis in HCC VM and metastasis, providing potential therapeutic targets. - Source: PubMed
Publication date: 2025/11/25
Wu ShilunYao ChangyuFang LuSun YiwenZhao MingmingChen JieHu GaofeiZhao ZheDing ShusiXue JingLiu XiaoyiSun WenbingKong JianZheng Lemin - Cervical cancer remains a significant health burden for women worldwide, with persistent high-risk HPV infection being a major etiological factor. Despite treatment advances, prognosis for recurrent or metastatic disease remains poor. Pyroptosis, a form of programmed cell death, plays a dual role in tumor immunity, but its implications in cervical cancer are not fully elucidated. This study aims to systematically characterize pyroptosis-related genes (PRGs) in cervical cancer and explore their prognostic and therapeutic relevance. - Source: PubMed
Yao ShijieChen SimingWan ShimengWang AnjinLiang ZiyanLiu XuelianGao YangCai Hongbing - The free fatty acid receptor FFAR4 is expressed in pancreatic islets, and its activation potentiates insulin and inhibits somatostatin (SST) secretion. We investigated the mechanisms of action of FFAR4 on hormone secretion in mouse and human islets. The effects of the FFAR4 agonist Compound A (Cpd A) on insulin and SST secretion were investigated in islets from mice following ablation of δ cells, deletion of SST and deletion of the G protein Gα ( ), in purified mouse β and δ cells, in human EndoC-bH5 cells, and in human islets. Ca dynamics in response to Cpd A were measured in δ cells from mouse islets and in human islets. The insulinotropic effect of Cpd A was lost in δ cell-ablated and SST-deficient mouse islets and was absent in purified mouse β cells. Gα deletion prevented Cpd A inhibition of SST secretion but not the potentiation of insulin release. Cpd A diminished Ca transients in mouse δ cells, an effect that was lost in Gα deficient islets. In human islets, FFAR4 activation increased insulin secretion and intracellular Ca transient independent of SST secretion. Consistent with a direct effect on β cells, Cpd A potentiated insulin secretion in human EndoC-βH5 cells. We conclude that FFAR4 activation stimulates insulin secretion from mouse islets indirectly via Gα-coupled inhibition of SST secretion from δ cells, while in human islets, it stimulates insulin release via a direct effect on β cells. These key species-related differences are to be taken into account as FFAR4 is considered a potential therapeutic target for metabolic diseases. - Source: PubMed
Publication date: 2025/08/18
Reininger LauraRehman MuhammadBouabcha AméliaFerragne SarahTremblay CarolineEthier MélanieKimple Michelle EGhislain JulienHuising Mark OPoitout Vincent - Prostate cancer (PCa) ranks among the most prevalent cancers in men, noted for its high mortality rate and unfavorable prognosis. Estrogen-related genes (ERGs) are significantly associated with the progression of PCa. This investigation aims to comprehensively assess the prognosis of PCa based on ERGs and explore its underlying biological mechanisms. Univariate, multivariate, and Least Absolute Shrinkage and Selection Operator (LASSO) regression analyses were conducted to identify prognostic signature genes and build a prognostic model. The model's predictive performance was assessed using Receiver Operating Characteristic (ROC) curve analysis. Gene Set Enrichment Analysis (GSEA), Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were employed to investigate the underlying molecular mechanisms of PCa. Antitumor drugs with high sensitivity were predicted using the CellMiner database and the pRRophitic package. Additionally, miRNAs targeting the identified signature genes were predicted using the miRNet database. This study identified six ERGs as prognostic biomarkers for PCa: POU4F1, BMP2, PGF, GAS1, GNAZ, and FGF11. The findings indicated that individuals in the low-risk category exhibited improved prognostic results. Notably, PCa progression may be closely linked to the cell adhesion molecule pathway and epigenetic regulation. Additionally, hsa-let-7a-5p and hsa-miR-34a-5p were identified as potential therapeutic regulators for PCa treatment. In conclusion, this research offers novel perspectives into the progression of PCa, providing robust scientific support for the development of personalized treatment strategies for PCa patients. - Source: PubMed
Publication date: 2025/04/10
Zhang HengFan Meng-DieHu YangYang QingJiang Jia-WeiXu Min - Diffuse large B-cell lymphoma (DLBCL) is an aggressive hematopoietic neoplasm that affects humans as well as dogs. While previous studies on canine DLBCL (cDLBCL) have significantly advanced our understanding of the disease, the majority of this research has relied on whole-exome sequencing, which is limited in its ability to detect copy number aberrations and other genomic changes beyond coding regions. Furthermore, many of these studies lack sufficient clinical follow-up data, making it difficult to draw meaningful associations between genetic variants and patient outcomes. Our study aimed to characterize the mutational landscape of cDLBCL using whole-genome sequencing of matched tumor-normal samples obtained from a cohort of 43 dogs previously enrolled in a clinical trial for which longitudinal follow-up was available. We focused on identifying genes that were significantly or recurrently mutated with coding point mutations, copy number aberrations, and their associations with patient outcomes. We identified 26 recurrently mutated genes, 18 copy number gains, and 8 copy number losses. Consistent with prior studies, the most commonly mutated genes included TRAF3, FBXW7, POT1, TP53, SETD2, DDX3X and TBL1XR1. The most prominent copy number gain occurred on chromosome 13, overlapping key oncogenes such as MYC and KIT, while the most frequent deletion was a focal loss on chromosome 26, encompassing IGL, PRAME, GNAZ, RAB36, RSPH14, and ZNF280B. Notably, our set of recurrently mutated genes was significantly enriched with genes involved in epigenetic regulation. In particular, we identified hotspot mutations in two histone genes, H3C8, and LOC119877878, resulting in H3K27M alterations predicted to dysregulate gene expression. Finally, a survival analysis revealed that H3K27M mutations in H3C8 were associated with increased hazard ratios for progression-free survival. No copy number aberrations were associated with survival. These findings underscore the critical role of epigenetic dysregulation in cDLBCL and affirm the dog as a relevant large animal model for interrogating the biological activity of novel histone-modifying treatment strategies. - Source: PubMed
Publication date: 2025/02/08
van der Heiden Anna DarlenePensch RaphaelaAgger SophieGardner Heather LHendricks WilliamZismann VictoriaWong ShukmeiBriones NataliaTurner BryceForsberg-Nilsson KarinLondon CherylLindblad-Toh KerstinArendt Maja Louise