ADCY8
- Known as:
- ADCY8
- Catalog number:
- 001199A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADCY8
Related genes to: ADCY8
- Gene:
- ADCY8 NIH gene
- Name:
- adenylate cyclase 8
- Previous symbol:
- ADCY3
- Synonyms:
- HBAC1, AC8
- Chromosome:
- 8q24.22
- Locus Type:
- gene with protein product
- Date approved:
- 1993-02-11
- Date modifiied:
- 2016-10-05
Related products to: ADCY8
Related articles to: ADCY8
- Normal follicular development forms the foundation for female reproductive performance, a process critically supported by angiogenesis. However, vascular endothelial zinc finger 1 (VEZF1), a key transcription factor regulating angiogenesis, was unexpectedly found to negatively regulate the survival of porcine ovarian granulosa cells (GCs) in our previous study. This study aimed to further explore whether and how VEZF1 regulates porcine GC growth. Using cell cycle analysis, cell proliferation assays, and RNA-seq analysis, we found that VEZF1 expression was significantly downregulated during follicular development (p < 0.01). Overexpression of VEZF1 arrested the cell cycle at the G0/G1 phase, reduced the proportion of S-phase cells, and inhibited cell proliferation (p < 0.05), whereas knockdown of VEZF1 exerted the opposite effects. Overexpression of VEZF1 downregulated Cytochrome P450 family 19 subfamily A member 1 (CYP19A1), but upregulated Cytochrome P450 family 11 subfamily A member 1 (CYP11A1) and Steroidogenic acute regulatory protein (STAR) protein expression, accompanied by increased progesterone levels. Mechanistically, VEZF1 activated the cAMP/PKA signaling pathway through upregulating luteinizing hormone/choriogonadotropin receptor (LHCGR) and adenylate cyclase 8 (ADCY8). In summary, this study demonstrated that VEZF1 acts as a negative regulator of GC proliferation, and its overexpression induces premature luteinization of GCs accompanied by the loss of proliferative activity. These findings establish VEZF1 as a key regulator of follicular development and lay the foundation for further exploring the application of VEZF1 in regulating reproductive performance in sows. - Source: PubMed
Publication date: 2026/05/25
Sun JingxinLi JialongLiu YiWang LuyaoWang HaifeiWu ShenglongBao WenbinJiang Aiwen - Neonicotinoid insecticides and fluoroquinolone antibiotics frequently co-occur in aquatic and terrestrial environments, posing a threat to human health, yet their combined neurotoxic potential remains poorly characterized. This study aimed to assess the cytotoxicity of typical neonicotinoids and fluoroquinolones as well as their mixtures in human neuroblastoma SK-N-SH cells and identify affected pathways. SK-N-SH cells were exposed to clothianidin (CLO), imidacloprid (IMI), enrofloxacin (ENR), and ofloxacin (OFX) individually and in fixed-ratio mixtures (50% of each compound's IC) for 24 h and 48 h, and cell viability was quantified using the alamarBlue method. Single-compound dose-response testing showed time-dependent cytotoxicity, with higher potency for fluoroquinolones (24 h IC: ENR 1.446 mM, OFX 2.742 mM; 48 h IC: ENR 0.826 mM, OFX 2.005 mM) than neonicotinoids (24 h IC: IMI 4.754 mM, CLO 5.356 mM; 48 h IC: IMI 3.631 mM, CLO 4.029 mM). Concentration-addition analysis indicated that most mixtures produced synergistic interaction in reduction in cell viability, with ENR+OFX showing the strongest effect at 48 h (Observed viability 7.138% vs. Predicated viability 82.368%). RNA-seq (24 h) revealed that binary mixtures generally induced more differentially expressed genes than single exposures, and ENR-containing mixtures showed the largest transcriptomic shifts, enriching pathways related to cellular stress and injury as well as neuronal signaling and connectivity. RT-qPCR validated the changes in expressions of five key neurobiology-relevant genes (, , , and ). These findings highlight the importance of assessing insecticide-antibiotic mixtures when evaluating their hazards in environment. - Source: PubMed
Publication date: 2026/02/25
Yeerkenbieke GulijiaziWang TaoYang YunShi ShuaiLu Xiaoxia - Depression, a common neuropsychiatric disorder, profoundly disrupts individuals' daily lives. Although the pathogenesis of depression is intensively investigated for decades, its underlying mechanisms remain elusive. Here, dysfunctional adenylyl cyclase 8 (Adcy8) is identified as a critical risk factor for the development of depression. Adcy8 expression is selectively decreased in the hippocampus, but not in the cortex, thalamus, and hypothalamus, of mice exposed to chronic stress. Adcy8 conditional knockout (CKO) in excitatory neurons, particularly dorsal CA1 (dCA1) neurons, resulted in pronounced depressive-like behaviors. Depletion of Adcy8 in dCA1 neurons reduces neuronal excitability and glutamatergic neurotransmission. Further mechanistic studies reveal a remarkable inhibition of the mitogen-activated protein kinase (MAPK) signaling pathway by Adcy8 CKO, which downregulates parathyroid hormone 2 receptor (PTH2R) level in the hippocampus. Knocking down Pth2r with AAV-shRNA duplicates the impairments in neuronal excitability, glutamatergic neurotransmission and depressive-like behaviors. In contrast, overexpression of PTH2R in Adcy8 CKO hippocampus rescues these deficits. Chronic infusion of TIP39, the endogenous ligand for PTH2R, into the hippocampus also alleviates depressive-like behaviors of Adcy8 CKO mice. Taken together, these results uncover critical roles of Adcy8 in suppressing depressive-like behaviors, likely by maintaining the excitability and glutamatergic neurotransmission of dCA1 neurons through TIP39-PTH2R signaling pathway. - Source: PubMed
Publication date: 2025/12/12
Liu Zi-JieBi Jia-RuiYu Zong-YanTian MengChen Zhi-YueWei RanWang Miao-MiaoZha Hai-WeiZhang Yu-QingWang Hong-JingQiang Bang-YouSun Shuang-ShuangZhu Xiao-JuanChen Wen-BingSun Dong - Ghrelin is a peptide hormone primarily produced by ghrelin cells in the stomach, playing a vital role in the regulation of eating behavior. Adenyl cyclase 8 (ADCY8), a key downstream signaling factor of G protein-coupled receptors, is essential for maintaining energy homeostasis by modulating levels of cyclic adenosine monophosphate (cAMP). Nevertheless, how ADCY8 modulates ghrelin levels and affects food intake is not well understood. Our findings demonstrated that Adcy8 mice exhibited elevated levels of ghrelin and increased food consumption under both normal and high-fat diet conditions. These changes were associated with a reduction in the activity of the cAMP-PKA-mTOR signaling pathway within the gastric mucosa. The administration of the ghrelin receptor antagonist d-Lys-3-GH-releasing peptide-6 significantly decreased calorie intake in both wild-type and Adcy8 mice. Furthermore, forskolin was shown to inhibit ghrelin and calorie intake in normal mice, an effect that was absent in Adcy8 mice. Treatment with forskolin or overexpression of Adcy8 in both primary ghrelin-producing cells and mHypoE-42 cells resulted in decreased ghrelin levels, accompanied by activation of the cAMP-PKA-mTOR signaling pathway. Conversely, the use of the inhibitor SQ22536 or knockdown of Adcy8 produced opposing effects. In conclusion, gastric ADCY8 regulates the expression and secretion of ghrelin via the cAMP-PKA-mTOR signaling pathway, thereby influencing food intake. - Source: PubMed
Wu ShaohongDeng HandanYu RuiliYu QuanLi WeiZhao YawenYang KeGao LuyangXu Geyang - The Warburg effect is the reprogramming of cancer cells towards glycolytic metabolism, likely producing and releasing lactate into the tumor microenvironment. This lactate has been suggested to partly drive tumor growth by signaling through the lactate receptor, GPR81. Thus, reprogramming cancer cells away from glycolytic activity may be beneficial for cancer treatment. Here, we show that deletion of ADCY8 (coding for adenylyl cyclase 8; AC8) employing the CRISPR-Cas9 technology in U87MG glioma cells, changes the proteome of these cells through a system-wide transformation in expression of mitochondrial proteins. These changes shift the metabolic balance towards oxidative phosphorylation, as shown by an increase in oxygen consumption, an elevation in tricarboxylic acid cycle flux, and a concomitant decrease in glycolytic flux. This metabolic shift is likely driven by the absence of AC8-mediated transcriptional regulation and may suggest that inhibition of AC8 activity could hold therapeutic potential in the treatment of cancer. - Source: PubMed
Publication date: 2025/07/14
Jakobsen EmilBech Jacob MAndersen Jens VWesti Emil WLarsen Martin RSkotte Niels HMoreira José M AAldana Blanca IBak Lasse K