ADCY10
- Known as:
- ADCY10
- Catalog number:
- 001201A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADCY10
Ask about this productRelated genes to: ADCY10
- Gene:
- ADCY10 NIH gene
- Name:
- adenylate cyclase 10
- Previous symbol:
- -
- Synonyms:
- SAC, Sacy, SACI, HCA2, RP1-313L4.2
- Chromosome:
- 1q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2008-01-16
- Date modifiied:
- 2017-09-25
Related products to: ADCY10
Related articles to: ADCY10
- The role of the cAMP/PKA pathway in antiviral innate immunity, including during coronavirus infections, remains unclear. We discovered coronavirus N proteins initiate cAMP-ADCY10-PKA cascade. Cytoplasmic PKA activates STAT1 independently of canonical JAK/TYR2 signaling. Coronavirus N proteins, via a conserved arginine (e.g., PEDV R58, SARS-CoV-2 R92), directly bind and sequester PKA Cα into the nucleus to evade STAT1 activation. Using PEDV as a model, mutant viruses with N and N were generated. Wildtype PEDV infection suppressed STAT1 activation in cells expressing PKA Cα/PKA Cα deficient in STAT1 phosphorylation. However, in rXS0101- or rXS0101-infected cells, only PKA Cα expression inhibited STAT1 activation. Downregulation of STAT1 activation is accompanied with increased viral replication. This study first elaborates that PKA Cα activates STAT1 in the cytoplasm of infected cells distinctly from canonical JAK/STAT1 signaling, while coronaviruses evade this antiviral response by sequestering PKA Cα into the nucleus via direct N protein interaction. - Source: PubMed
Publication date: 2026/04/24
Xu JidongXiao YutingLu WanqingSong ZiyaoZhou LeiGao QinXu XiaohanShan YingFang WeihuanZhao LingyanLi Xiaoliang - Soluble adenylyl cyclase (sAC; ADCY10) is an evolutionarily ancient, intracellular source of cAMP that is molecularly and mechanistically distinct from the more widely studied, hormone-responsive, G protein regulated transmembrane adenylyl cyclases. Unlike other mammalian cyclases, sAC is most abundantly expressed in male germ cells and is directly regulated by bicarbonate and calcium. Genetic and pharmacological evidence in rodents and humans establishes sAC as essential for male fertility: loss of sAC activity yields immotile sperm incapable of fertilizing the egg resulting in male-specific infertility. These features position sAC as a promising target for developing nonhormonal, on-demand contraceptives suitable for men and women. A proof-of-concept inhibitor has demonstrated a rapid, reversible contraceptive effect in mice, but translation to a clinical product must address challenges inherent to on-demand sperm-targeted pharmacology. In addition to ensuring a high safety margin and navigating an emerging regulatory and commercial landscape, common to any male contraceptive, on-demand male contraception must define onset/duration of efficacy while ensuring persistent inactivation of sperm function after ejaculation. - Source: PubMed
Publication date: 2026/03/17
Gardner Erin RKopf Gregory SBuck JochenLevin Lonny R - cAMP is a ubiquitous second messenger produced from ATP and involved in many cellular processes. In humans, cAMP is produced from two types of adenylyl cyclases: G protein-regulated transmembrane adenylyl cyclases (ADCY1-9) and bicarbonate- (HCO) and calcium- (Ca) regulated soluble adenylyl cyclase (sAC; ADCY10). sAC is molecularly and biochemically distinct from other mammalian nucleotidyl cyclases. In most mammals, sAC arises from a single gene which is predicted to generate multiple isoforms via alternative splicing. In rodents, there are two molecularly identified splice variants: the "full-length" isoform (sAC) and a "truncated" isoform (sAC). To date, biochemical and structural characterization of sAC has focused almost exclusively on the sAC isoform. Longer sAC isoforms, including the longest known sAC, contain additional presumptive regulatory domains which have not yet been functionally characterized. Thus far, studies have been limited by the inability to obtain sufficient sAC protein to allow in vitro biochemical characterization. Here, we describe attempts to heterologously express and purify human sAC as well as generation of a novel genetically modified mouse strain which permits biochemical separation and purification of endogenously expressed mouse sAC and sAC. We use these heterologously expressed and endogenous proteins to compare and contrast the biochemically properties of human and mouse sAC and sAC. - Source: PubMed
Publication date: 2025/11/05
Ferreira JacobBelliveau HaydenLevin Lonny RBuck Jochen - β-Nicotinamide adenine dinucleotide (β-NAD) is recognized as a sympathetic neurotransmitter that relaxes vascular and intestinal smooth muscle through purinergic receptor pathways. In the lung, β-NAD has been associated with anti-inflammatory effects, but its role in regulating airway smooth muscle tone remains unexplored. This study investigates the impact of β-NAD on airway smooth muscle and elucidates the underlying mechanisms of its action. - Source: PubMed
Publication date: 2025/10/14
Jurastow InnokentijWiegand SilkeRafiq AmirZakrzewicz AnnaEngel SandraSanna Adrianovon der Beck DanielKlepetko WalterHecker AndreasGünther AndreasBünemann MoritzKrasteva-Christ GabrielaKeshavarz Maryam - This study investigated lipid metabolism differences between low and high residual feed intake (LRFI and HRFI) bulls. Fifty-five Simmental bulls (449.84 ± 8.49 kg) were fed the same diet for 161 d to determine RFI values. At the end of experiment, back fat thickness (BFT) and rib eye area (REA) were measured via ultrasound, and serum samples were collected for lipid metabolism indicators. Post-slaughter, subcutaneous adipose tissue was analyzed for lipid metabolism indicators, histology, transcriptomics, and lipid metabolomics. Results 1) Ultrasound showed LRFI bulls had lower BFT ( = 0.031) but higher REA ( = 0.021). 2) Serum total cholesterol ( = 0.028) and low-density lipoprotein cholesterol ( = 0.015) were lower in LRFI bulls. Leptin levels were lower in both serum ( = 0.007) and adipose tissue ( = 0.001) in LRFI bulls, as were acetyl-CoA carboxylase levels in serum ( = 0.032) and adipose tissue ( = 0.043). Conversely, adipose triglyceride lipase levels were higher in both serum ( = 0.045) and adipose tissue ( = 0.043), while adipose tissue fatty acid synthase levels were lower ( = 0.035) in LRFI bulls. 3) Transcriptomics identified two pathways, adenosine monophosphate-activated protein kinase (AMPK) and cyclic adenosine monophosphate (cAMP), involving five lipid metabolism-related genes. Among these, adenylate cyclase activating polypeptide 1 receptor type 1 (), adenylate cyclase 10 (), and adenylate cyclase activating polypeptide 1 () were significantly upregulated ( < 0.05), while leptin receptor () was downregulated ( = 0.047) in LRFI bulls. Additionally, leptin () showed a downward trend ( = 0.098) in LRFI bulls. 4) Lipid metabolomics revealed that the LRFI group had significantly higher levels of wax ester (WE) ( = 0.040) and significantly lower levels of monogalactosyldiacylglycerol (MGDG) ( = 0.040) compared to the HRFI group. Additionally, sphingomyelin (SPH) showed a trend towards lower abundance ( = 0.054), and C12:0 levels tended to be higher ( = 0.089) in the LRFI group. In conclusion, differences in the AMPK and cAMP signaling in adipose tissue are associated with reduced lipid synthesis and enhanced lipid degradation in LRFI bulls, which may contribute to reduced lipid deposition. - Source: PubMed
Publication date: 2025/07/12
Yi XinYi SimengWang JinzeYe BopingZhu XiaowenMeng QingxiangWu HaoZhou Zhenming