Ask about this productRelated genes to: SPATA12 Blocking Peptide
- Gene:
- SPATA12 NIH gene
- Name:
- spermatogenesis associated 12
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3p14.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-10-22
- Date modifiied:
- 2016-10-05
Related products to: SPATA12 Blocking Peptide
Related articles to: SPATA12 Blocking Peptide
- Spermatogenesis-associated gene 12 () functions as an inhibitor in spermatogenesis and tumorigenesis. Our previous study demonstrated that SPATA12 may be induced in tumor cells by ultraviolet (UV) C-mediated DNA damage, suggesting its importance in maintaining genomic integrity. In order to understand whether and how responds to oxidative damage, the present study established a cellular model of oxidative stress by detecting the effect of HO on cell viability and intracellular superoxide dismutase activity, and the levels of glutathione and malondialdehyde (MDA). Quantitative polymerase chain reaction results demonstrated that HO upregulated the expression of , and a dual luciferase reporter gene assay indicated that transcription factor activator protein-1 (AP-1) was involved in the response of to oxidative stress. Through the exogenous expression of , it was identified that decreased the level of reactive oxygen species and MDA, and also may reduce the degree of cellular oxidative damage and apoptosis induced by HO. In addition, resveratrol was demonstrated to increase the expression of by activating AP-1, and it may be used as a nontoxic activator of the gene. In conclusion, these results suggest that is upregulated by oxidative stress via AP-1, and that the exogenous expression of protects against HO-induced oxidative damage and apoptosis. - Source: PubMed
Publication date: 2018/01/08
Wu DaobingLi DanLiu ZhiyongLiu XiaowenZhou ShihuaDuan Hongyan - Environmental BPA exposure has been shown to impact human sperm concentration and motility, as well as rodent spermatogenesis. However, it is unclear whether BPA exposure is associated with alteration in DNA hydroxymethylation, a marker for epigenetic modification, in human sperm. A genome-wide DNA hydroxymethylation study was performed using sperm samples of men who were occupationally exposed to BPA. Compared with controls who had no occupational BPA exposure, the total levels of 5-hydroxymethylcytosine (5hmc) increased significantly (19.37% increase) in BPA-exposed men, with 72.69% of genome regions harboring 5hmc. A total of 9,610 differential 5hmc regions (DhMRs) were revealed in BPA-exposed men relative to controls, which were mainly located in intergenic and intron regions. These DhMRs were composed of 8,670 hyper-hMRs and 940 hypo-hMRs, affecting 2,008 genes and the repetitive elements. The hyper-hMRs affected genes were enriched in pathways associated with nervous system, development, cardiovascular diseases and signal transduction. Additionally, enrichment of 5hmc was observed in the promoters of eight maternally expressed imprinted genes in BPA-exposed sperm. Some of the BPA-affected genes, for example, MLH1, CHD2, SPATA12 and SPATA20 might participate in the response to DNA damage in germ cells caused by BPA. Our analysis showed that enrichment of 5hmc both in promoters and gene bodies is higher in the genes whose expression has been detected in human sperm than those whose expression is absent. Importantly, we observed that BPA exposure affected the 5hmc level in 11.4% of these genes expressed in sperm, and in 6.85% of the sperm genome. Finally, we also observed that BPA exposure tends to change the 5hmc enrichment in the genes which was previously reported to be distributed with the trimethylated Histone 3 (H3K27me3, H3K4me2 or H3K4me3) in sperm. Thus, these results suggest that BPA exposure likely interferes with gene expression via affecting DNA hydroxymethylation in a way partially dependent on trimethylation of H3 in human spermatogenesis. Our current study reveals a new mechanism by which BPA exposure reduces human sperm quality. - Source: PubMed
Publication date: 2017/06/05
Zheng HuajunZhou XiaoyuLi De-KunYang FenPan HongjieLi TianqiMiao MaohuaLi RunshengYuan Wei - Our previous studies indicated that SPATA12, a novel spermatogenesis-associated gene, might be an inhibitor involved in spermatogenesis and tumorigenesis. To obtain a better understanding of the functions of SPATA12, a yeast two-hybrid screening system was used to search for interacting proteins, and chromodomain helicase DNA binding protein 2 (CHD2) was successfully identified. Bimolecular fluorescence complementation (BiFC) and subcellular co-localization assays further suggested a possible interaction between SPATA12 and CHD2 in the nuclei. CHD2 is known to be involved in the later stage of the DNA damage response pathway by influencing the transcriptional activity of p53. Thus, our hypothesis is that SPATA12 might play a role in DNA damage signaling. Western blotting results showed that SPATA12 expression could be induced in ultraviolet-C (UV-C) irradiated cells. Through reporter gene assays and the activator protein-1 (AP-1) decoy oligodeoxynucleotide method, we demonstrated that SPATA12 promoter activity could be up-regulated in response to UV-C radiation exposure and an AP-1 binding site in the SPATA12 promoter may have a role in transcriptional regulation of SPATA12. Using colony formation and host cell reactivation assays, it was demonstrated that SPATA12 might lead to inhibition of cellular proliferation in UV-C-irradiated DNA damage. Furthermore, SPATA12 was transfected into H1299, MCF-7 and HeLa cells, and flow cytometry (FCM) results suggested that there are some biological association between SPATA12 and p53 in UV-C-irradiated DNA damage. In addition, we investigated whether SPATA12 could up-regulate the expression of p53. Taken together, these findings indicate that SPATA12 could be induced under UV-C stress. During DNA damage process, AP-1 involves in the transcriptional up-regulation of SPATA12 in response to UV-C radiation and p53 involves in growth inhibitory effects of SPATA12 on UV-C irradiated cells. - Source: PubMed
Publication date: 2013/10/18
Zhang YunshengYang LifangLin YitingRong ZhuoxianLiu XiaowenLi Dan - The unique differentiation mechanisms of spermatogenesis suggest the existence of cell type- and stage-specific molecules. Herein, a microarray-based approach was used to identify changes in the gene expression profile in mouse GC-1 spg germ cells transfected with spermatogenesis associated gene 12 (SPATA12). One hundred and eighty-two upregulated genes and 104 downregulated genes with fold changes of ≥2 or ≤0.5 (P≤0.05) in expression were identified. Ten genes were selected for validation of the microarray results using quantitative RT-PCR. The real-time quantitative RT-PCR results were consistent with that of the microarray. The gene ontology (GO) terms for the biological functions of the differentially expressed genes induced by SPATA12 included binding activity and immune response. Biological pathway analysis identified several related pathways which are associated with immune responses, cell adhesion and the developmental process. In addition, we observed that SPATA12 may interact with the β-catenin signaling pathway and that SPATA12 may negatively regulate β-catenin signaling during spermatogenesis. - Source: PubMed
Publication date: 2012/12/27
Lin YitingLiu ZhiwenLiu XuanmingZhang YunshengRong ZhuoxianLi Dan - Human SPATA12 is a spermatogenesis associated gene and is supposed to function as an inhibitor during male germ cell development. SPATA12 is specifically expressed in spermatocytes, spermatids, and spermatozoa of human testis. In order to understand the regulation mechanism of SPATA12 gene expression, we identified and characterized the SPATA12 gene core promoter region and transcription factor binding sites by using reporter gene assays. AP-1 is founded to be a potential transcriptional activator of SPATA12. The promoter activity of SPATA12 was drastically declined after AP-1 binding site mutation or deletion. We also demonstrated that AP-1 combined with Smad3/4 contributes to the transcriptional regulation of SPATA12 in response to TGF-β1. The expression of SPATA12 could be induced by TGF-β1 in a dose-dependent manner, suggesting that AP-1 as an activator plays a role in the regulation of SPATA12 promoter. We have also shown that heat shock treatment could activate the expression of SPATA12 and transcription factor HSF binding sites in the SPATA12 promoter might be responsible for this heat-induction. These results suggested that AP-1 and HSF may play an important role in regulating SPATA12 promoter activity. - Source: PubMed
Publication date: 2012/09/05
Li DanLin YitingLiu ZhiwenZhang YunshengRong ZhuoxianLiu Xuanming