Ask about this productRelated genes to: GOLGA7 antibody
- Gene:
- GOLGA7 NIH gene
- Name:
- golgin A7
- Previous symbol:
- -
- Synonyms:
- GCP16, HSPC041, GOLGA3AP1, GOLGA7A
- Chromosome:
- 8p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-23
- Date modifiied:
- 2019-03-12
Related products to: GOLGA7 antibody
Related articles to: GOLGA7 antibody
- Crossbreeding indigenous cattle with high-yielding exotic breeds has been a key strategy in Indian dairy systems for increasing milk production. The Karan Fries (KF), a stabilised dairy cattle population derived from the Tharparkar and Holstein Friesian breeds, serves as a valuable genetic resource in India. Despite their adaptability and performance, the genomic architecture underpinning milk traits and stature in KF cattle remains largely unexplored. Therefore, a genome-wide association study (GWAS) was conducted using 777 K SNP genotyping data and estimated breeding values (EBVs) as the dependent variable for four economically important dairy traits: first lactation total milk yield (FLTMY), total fat yield (TFY), total solids-not-fat yield (TSNFY), and stature. After quality control and LD pruning, 347,621 SNPs across 355 KF animals were analysed, revealing 54 significant single-nucleotide polymorphisms (SNPs) associated with these traits, with several exhibiting pleiotropic effects. Candidate genes such as EPHA7, SCFD2, DCUN1D4, CWH43, ZMAT4, KYNU, GINS4, GPAT4, GOLGA7, and OCIAD1 were associated with milk yield and compositional traits, while CBLB, CCDC14, ALCAM, MALRD1, and MUC13 were linked to stature. Protein-protein interaction network analysis identified functionally connected gene clusters involved in lactation, fat metabolism, and structural development. These results provide preliminary insights into the genomic architecture of KF cattle and highlight candidate genes associated with milk production and stature traits. While exploratory in nature, these findings may serve as a starting point for future validation and the development of genomic selection strategies in tropical dairy cattle. - Source: PubMed
Publication date: 2026/02/05
Pal PritamKumar IshmeetChoudhary ManishaUpadhyay AmritanshuIlayaraja IrusappanChitra AnilMuansangi LalGowane GopalRaja T VMukherjee AnupamaMukherjee Sabyasachi - Small molecules serve as valuable tools for probing nonapoptotic cell death mechanisms. The small molecule caspase independent lethal 56 (CIL56) induces a unique form of nonapoptotic cancer cell death that is promoted by a complex formed between zDHHC palmitoyltransferase 5 (ZDHHC5) and an accessory protein, golgin A7 (GOLGA7, also known as GCP16). The structure and function of this complex in nonapoptotic cell death regulation remain poorly understood. Here, we use coimmunoprecipitation, functional assays, and cryogenic electron microscopy (cryo-EM) to elucidate the structure and function of the Zdhhc5-GOLGA7 complex. We identify key residues in both Zdhhc5 and GOLGA7 that are necessary for complex formation and to promote nonapoptotic cancer cell death in response to caspase independent lethal 56. These results provide new insights into the structure and function of a death-promoting protein complex. - Source: PubMed
Publication date: 2025/09/08
Kahlson Martha ARitho JoanGomes João VictorWang HaoqingButterwick Joel ADixon Scott J - NRAS mutations are prevalent in human hematological malignancies and are also common in certain solid tumors, including melanoma and colon cancer. Despite their crucial role in oncogenesis, no effective therapies targeting NRAS have been developed. Inhibiting NRAS localization to the plasma membrane (PM) represents a promising strategy for cancer therapy, as its oncogenic signaling relies on PM localization. Knocking out Golgin subfamily A member 7 (Golga7), an accessory protein of RAS palmitoyltransferases, through a conditional gene editing approach drastically suppresses the development of myeloid leukemia induced by the activation of Nras knock-in alleles in mice. The loss of Golga7 disrupts NRAS PM localization in bone marrow cells without altering the level of NRAS palmitoylation. Notably, Golga7 is dispensable for normal hematopoiesis in adult mice. While constitutive Golga7 knockout leads to embryonic lethality, the ubiquitous knockout of Golga7 induced in adult mice does not manifest any measurable toxic effects. These findings indicate that GOLGA7 is an effective and safe therapeutic target for NRAS-driven leukemias. - Source: PubMed
Publication date: 2025/03/17
Jiao BoYan LeiZhang RuiHuang WeiWang XinruLiu ChenxuanWang PeihongXu PengfeiWang JinzengFang ZhouLi DongheXia ZhizhouLi JiaoyangJi ShiyuZhang QianqianWu MinWang ShengyueLiu PingRen Ruibao - Ammonia, a common toxic gas, posed a hazard to both human and chickens. The Golgi apparatus, an essential organelle, helped maintain the internal environment of the organism and supported the protein foundation for the endoplasmic reticulum to be involved in pyroptosis. Thus, the Golgi apparatus has garnered significant attention. The purpose of our research was to explore the mechanisms of Golgin A7 (Golga7) involved in pyroptosis after chicken exposure to ammonia. To reach our goal, we first created an in vitro ammonia model to study the effect of ammonia on chicken splenic lymphocyte pyroptosis. Then, leveraging this model, we established Golga7 and miR-32-5p knockdown and overexpression models to investigate their roles in ammonia-induced pyroptosis. We found the ultrastructural changes in the nucleus, Golgi apparatus, and mitochondria of chicken splenic lymphocytes exposure to ammonia. The damage of mitochondria increased the level of Reactive Oxygen Species (ROS), which caused the down-regulation of miR-32-5p. The miR-32-5p inhibitor increased the expression of Golga7 and pyroptosis-related genes (NOD-like receptor protein 3 (NLRP3), Cysteine aspartase-1 (Caspase-1), Golgin A3 (Golga3), Nuclear Factor-kappa B (NF-κB), and Tumor Necrosis Factor-alpha (TNF-α)), which induced the pyroptosis, but when miR-32-5p mimic/si-Golga7 (Golga7 inhibitor) was utilized, these effects were reduced. Our research demonstrated that miR-32-5p/Golga7 regulated NLRP3 involving in the pyroptosis of chicken splenic cells exposed to ammonia. Our study provided a valuable foundation for the prevention and treatment chickens ammonia poisoning in the livestock production. - Source: PubMed
Publication date: 2024/09/12
Liu JiahaoLiu HaifengTang HaojinmingRan LongjunWang DanniYang FalongZhang HuanrongTeng XiaohuaChen Dechun - During maturation oocytes at the germinal vesicle (GV) stage progress to metaphase II (MII). However, during in vitro maturation a proportion often fail to progress. To understand these processes, we employed RNA sequencing to examine the transcriptome profile of these three groups of oocytes from the pig. We compared our findings with similar public oocyte data from humans. The transcriptomes in oocytes that failed to progress was similar to those that did. We found in both species, the most upregulated genes in MII oocytes were associated with chromosome segregation and cell cycle processes, while the most down regulated genes were relevant to ribosomal and mitochondrial pathways. Moreover, those genes involved in chromosome segregation during GV to MII transition were conserved in pig and human. We also compared MII and GV oocyte transcriptomes at the isoform transcript level in both species. Several thousands of genes (including DTNBP1, MAPK1, RAB35, GOLGA7, ATP1A1 and ATP2B1) identified as not different in expression at a gene transcript level were found to have differences in isoform transcript levels. Many of these genes were involved in ATPase-dependent or GTPase-dependent intracellular transport in pig and human, respectively. In conclusion, our study suggests the failure to progress to MII in vitro may not be regulated at the level of the genome and that many genes are differentially regulated at the isoform level, particular those involved ATPase- or GTPase-dependent intracellular transport. - Source: PubMed
Publication date: 2024/08/09
Tang FengHummitzsch KatjaRodgers Raymond J