ADCY7
- Known as:
- ADCY7
- Catalog number:
- 001198A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADCY7
Related genes to: ADCY7
- Gene:
- ADCY7 NIH gene
- Name:
- adenylate cyclase 7
- Previous symbol:
- -
- Synonyms:
- KIAA0037, AC7
- Chromosome:
- 16q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-22
- Date modifiied:
- 2015-09-11
Related products to: ADCY7
Related articles to: ADCY7
- Calcium signaling, as a ubiquitous intracellular signal in eukaryotes, has been impacted in multiple biological processes encompassing tumorigenesis. Nevertheless, the integrated investigations on the function and prognostic value of genes correlated to calcium signaling in bladder cancer (BLCA) were still lacking. - Source: PubMed
Publication date: 2026/02/06
Zhang LuluGong YuChen JiajunLi MengyaoWang XiurongWang WeihaoDing QiannanLi Yulei - The association between early life exposure to smoking and the risk of inflammatory bowel disease (IBD) needs to be further verified, and the potential role of DNA methylation in the association is unclear. Through an integrated study design, this study demonstrates that maternal smoking during pregnancy (MSDP) is potentially associated with increased risk of IBD, Crohn's disease (CD), and ulcerative colitis (UC) in offspring. In addition, individuals who started smoking in adolescence have a higher risk of developing CD and IBD. Mechanistically, MSDP-associated DNA methylation alterations in ADCY7 (newborn), AKAP8L (newborn), TIGD7 (newborn), and TNF/LTA (across life stages) are significantly correlated with increased risk of CD in offspring; MSDP-induced DNA methylation changes in PRRT1 (newborn), AHRR (across life stages), and MYO1G (across life stages) show significant associations with UC risk in offspring. Notably, the alterations of DNA methylation status within AHRR, MYO1G, and TNF/LTA loci associated with smoking exposure are present throughout the life course. Collectively, MSDP may serve as an independent risk factor for IBD in offspring, and active smoking during adolescence may cause increased risk of developing CD and IBD. MSDP may contribute to IBD susceptibility by inducing persistent DNA methylation alterations at multiple developmental stages. - Source: PubMed
Publication date: 2026/01/11
Zhang HanZhao JianhuiChen JieMa XinyiZhou SiyunNoble AlexandraKalla RahulWellens JudithLiu KunTheodoratou EvropiSatsangi JackLi Xue - Coat color represents a key phenotypic trait in Sibu yak, exhibiting distinct black and brown phenotypes. To elucidate the genetic basis of the brown phenotype, genome-wide association studies and multi-omics analyses were integrated to identify loci and molecular pathways involved in pigmentation. In total, 11 single-nucleotide polymorphisms (SNPs) on chromosome (chr) 5 displayed genome-wide significance ( -adjust<4.47×10 ), with the lead variant (chr5: g.47487664 A>G, -adjust=2.38×10 ) located within an intron of . Expression analysis revealed markedly reduced transcription in fibroblasts from brown individuals. Functional multi-omics analyses of overexpression demonstrated significant alteration of the expression of 1 088 genes, 444 proteins, and 57 metabolites. Enrichment analyses indicated significant involvement of melanogenesis-related signaling cascades, including cAMP (e.g., , EDNRA, and epinephrine), PI3K-Akt (e.g., , , and FGF7), and MAPK (e.g., , , and ERBB4) pathways. These findings indicate that the intronic variant modulates gene expression and pigmentation through coordinated regulation of these pathways, thereby contributing to the phenotypic divergence of Sibu yak coat color. This study provides valuable insights into the genetic mechanisms underlying Sibu yak pigmentation and identifies as a key candidate gene governing coat color differentiation in Sibu yak. - Source: PubMed
Zhang Hao-YuanXu LuWang Jin-HuanCeccobelli SimoneZhu YongZhang QiangZhang Cheng-FuHu Peng-FeiLiu Cheng-LiYang Bai-GaoRuan Peng-ChengRen TaoCong HeZeng YanHan Yan-GuoWang Shi-ZhiZhao Yong-JuZhao Zhong-QuanHuang Yong-FuNie Wen-HuiE Guang-Xin - Rheumatoid arthritis (RA) is a prevalent autoimmune disorder that significantly reduces quality of life and imposes a substantial burden on society. This study addresses the critical gaps in current diagnostic and therapeutic modalities by aiming to identify improved biomarkers and potential therapeutic targets. Using data from 2 gene expression omnibus databases, we executed a comprehensive differential gene expression analysis integrated with Mendelian randomization. This approach employed advanced bioinformatics tools to scrutinize expression quantitative trait loci (eQTLs) and RA genome-wide association study data to pinpoint crucial genes involved in RA. The selection of these pivotal genes was strategically based on the intersection of upregulated gene expressions with eQTLs exhibiting odds ratios >1, and conversely, downregulated gene expressions aligned with eQTLs displaying odds ratios <1. Our enrichment analyses, including gene ontology, Kyoto encyclopedia of genes and genomes, and gene set enrichment analysis, provided robust validation of these genes' roles, further supported by external validation from an additional gene expression omnibus dataset. The study identified 13 critical genes related to RA susceptibility, including CKAP2, GABBR1, HLA-DPA1, ST6GAL1, FCGR1A, ADCY7, MAP4K1, CD37, ERAP2, and SEMA3C, alongside protective genes. An in-depth analysis of immune cell infiltration underscored the dominant roles of M2 macrophages and CD8+ T cells in the RA immune microenvironment, highlighting their significant contributions to disease pathogenesis. By identifying novel biomarkers and elucidating the dynamic immune landscape of RA, our findings lay the groundwork for innovative therapeutic strategies. This study significantly advances our understanding of the complex genetic mechanisms underlying RA, offering insights that pave the way for targeted therapeutic interventions and further research into the molecular drivers of RA. - Source: PubMed
Shao ShoujiaZeng WenxingZhang JingtaoMa LuyaoHuang FengJiang Ziwei - Toll-like receptor 9 (TLR9) agonists cause activation of nucleotide-binding domain, leucine-rich repeat protein 3 (NLRP3) inflammasomes but the mechanism is not clear. We found that there is a second signal downstream of TLR9 that induces NLRP3 inflammasome activation. Through screening, adenylate cyclase 7 (ADCY7) was found to be an essential regulator of this process. In cells with Adcy7 deficiency, TLR9 agonists were no longer able to activate the NLRP3 inflammasome. ADCY7 not only catalyzes the generation of cyclic adenosine monophosphate (cAMP) but also catalyzes the synthesis of its dimeric form (c-di-AMP). Moreover, c-di-AMP promotes assembly and maturation of the inflammasome by directly binding to NLRP3. Cells with Adcy7 deletion or mutations impacting enzymatic activity cannot produce c-di-AMP. The survival of Adcy7-deficient mice in acute liver injury was also improved. In summary, we found that ADCY7 is required for NLRP3 inflammasome activation downstream of TLR9 by catalyzing the generation of c-di-AMP, which may serve as a target for controlling inflammatory responses in sterile infections. - Source: PubMed
Publication date: 2025/05/26
Liu QiannvTang ZhihengQian YanWang ChunleiKong ChunLi MengqianGeng XiangyangZhang YanCheng XiangyunRen ChaoWang KaiBai LinWang LinJiang DongWang ShuoLiu XiaoyunXia Pengyan