Ask about this productRelated genes to: GNAZ Blocking Peptide
- 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 Blocking Peptide
Related articles to: GNAZ Blocking Peptide
- Hepatocellular carcinoma (HCC) is a highly heterogeneous malignancy, and its intrinsic variability contributes to aggressive progression, recurrence, and therapeutic resistance. Exosomes are key mediators of intercellular communication among tumor cells with different malignant potentials, while N6-methyladenosine (mA) modification has emerged as a critical epigenetic regulator of tumorigenesis. However, the mechanisms by which exosome-mediated mA regulation contributes to HCC progression and heterogeneity remain poorly understood. - Source: PubMed
Publication date: 2026/07/29
Wei YiHan Shen-QiXue LinXiong Zhi-Fan - As a key index of reproductive performance in pigs, gestation length (GL) exerts a direct influence on litter size and the survival rate of piglets. Phenotypic variability in GL has been observed across Large White pig populations. To elucidate the genetic mechanisms underlying GL, this study analyzed 22,783 reproductive records from 9,057 pigs across five Large White populations. We employed a combination of diverse analytical strategies, encompassing genome-wide association studies (GWAS), GWAS meta-analysis, Bayesian fine-mapping (BFM), transcriptome-wide association studies (TWAS), phenome-wide association studies (PheWAS), and epigenetic profiling. - Source: PubMed
Publication date: 2026/06/10
Zhou JinZhao QingboQian XiaowenZeng TaoXu LimingLiu QianYin YanzhenMa JinfengYu JianghuiJiang ZhengZhao GuankaiHuang RuihuaLi Pinghua - 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