| 1998 |
Human ADCY9 (AC9) is stimulated by beta-adrenergic receptor activation but is insensitive to forskolin, Ca2+, and somatostatin when expressed in HEK-293 cells; unlike mouse AC9, human AC9 activity is unaffected by inhibitors of calcineurin. Divergence at the C2a/C2b junction results in an alternative C2b amino acid sequence compared to mouse AC9. |
Heterologous expression in HEK-293 cells, pharmacological assays, cAMP measurement |
Genomics |
Medium |
9628827
|
| 2008 |
miR-142-3p targets AC9 mRNA to suppress cAMP production in CD4+CD25- T cells; in CD4+CD25+ T regulatory cells, FOXP3 downregulates miR-142-3p, thereby keeping the AC9/cAMP pathway active and enabling high cAMP levels required for suppressor function. |
miRNA target validation (luciferase reporter, mRNA/protein quantification), T cell functional assays, cAMP measurement, FOXP3 overexpression/knockdown |
EMBO reports |
High |
19098714
|
| 2013 |
miR-181b targets AC9 mRNA to restrict cAMP production post-transcriptionally in cervical cancer cells; knockdown of AC9 phenocopies miR-181b overexpression (increased proliferation, reduced apoptosis), while AC9 overexpression has opposite effects. |
miRNA target validation (luciferase reporter assay), siRNA knockdown and overexpression, cAMP measurement, proliferation and apoptosis assays |
FEBS letters |
Medium |
24269684
|
| 2014 |
AC9 catalyzes cAMP production in APL cells and enhances retinoic acid receptor trans-activity; AC9 knockdown inhibits ATRA-induced differentiation of NB4 cells. miR-181a targets the 3'UTR of AC9 mRNA to decrease AC9 expression and intracellular cAMP, and CEBPα inhibits miR-181a expression, accounting for differential AC9 levels between ATRA-sensitive and resistant cells. |
Luciferase reporter assay (3'UTR targeting), siRNA knockdown, overexpression, cAMP measurement, differentiation assays, CEBPα gain/loss of function |
Cell death & disease |
Medium |
24722286
|
| 2018 |
The isoform-specific carboxyl-terminal C2b domain of AC9 auto-inhibits enzyme activation by Gs-coupled receptors; deletion of the C2b domain markedly enhances cAMP response to beta-adrenergic and prostanoid receptor activation. Residues 1268-1276 within C2b are critical for auto-inhibition. Two molecular weight species of AC9 (~130K and ≥170K) are detected in myocardial membranes, with the lower species lacking the C2b domain, suggesting proteolytic cleavage may regulate AC9 activity. |
Deletion mutagenesis, stable overexpression in HEK-293 cells, cAMP assay, immunoblotting with domain-specific antibodies, rodent and human myocardial membrane fractionation |
Cellular signalling |
High |
30121334
|
| 2018 |
Adcy9 inactivation in mice reduces aortic atherosclerosis by 65%, decreases macrophage accumulation and proliferation in plaques, and improves endothelial-dependent vasorelaxation via nitric oxide, cyclooxygenase, and endothelial-dependent hyperpolarization pathways. These protective effects are entirely lost when CETP is present (CETPtg Adcy9Gt/Gt mice), demonstrating that Adcy9 inactivation protects from atherosclerosis only in the absence of CETP activity. |
Genetic inactivation (Adcy9Gt/Gt mice), atherogenic diet protocol, histology (CD68 macrophage staining), vasorelaxation pharmacology, telemetry, adipose tissue MRI, splenocyte adhesion assay |
Circulation |
High |
29674325
|
| 2019 |
miR-142-3p targets AC9 in dorsal root ganglion/spinal cord neurons; miR-142-3p inhibition upregulates AC9, elevates cAMP and downstream p-CREB, IL-6, and GAP43, and reduces GTP-RhoA, promoting axon growth in vitro and sensory conduction recovery in vivo after dorsal column injury. Co-knockdown of AC9 reverses these effects. Sorafenib mimics SNCI by downregulating miR-142-3p. |
miR-142-3p inhibitor/mimic delivery in rats, AC9 siRNA, axon length measurement, cAMP/protein quantification, in vivo sensory conduction electrophysiology |
Neuropharmacology |
Medium |
30710569
|
| 2020 |
miR-142-3p directly targets AC9 (validated by luciferase reporter assay) in sciatic nerve injury (CCI) rats; miR-142-3p expression increases while AC9 and cAMP decrease in CCI rats. miR-142-3p silencing reduces neuropathic pain and inflammatory cytokines via upregulation of AC9 and downstream cAMP/AMPK pathway proteins. |
Dual luciferase reporter assay, miR-142-3p mimic/siRNA delivery in CCI rats, AC9 overexpression/siRNA, cAMP measurement, AMPK pathway protein quantification, pain behavioral testing |
International journal of molecular medicine |
Medium |
33416140
|
| 2020 |
Deletion of adcy9 in zebrafish (morphant model) causes cardiac malformation with increased macrophage migration, cardiac apoptosis, and upregulation of mmp9 (matrix metalloproteinase involved in extracellular matrix remodeling), supporting ADCY9 as a candidate gene for congenital heart defects. |
Zebrafish adcy9 morpholino knockdown, immunofluorescence (macrophage markers), RNA sequencing, cardiac morphology assessment |
Orphanet journal of rare diseases |
Medium |
32321550
|
| 2022 |
miR-210-3p targets ADCY9 mRNA (validated by target relation detection); miR-210-3p is downregulated while ADCY9 is upregulated in myocardial infarction rats. Sevoflurane-mediated cardioprotection (reduced injury, fibrosis, and apoptosis) is potentiated by miR-210-3p elevation and abolished by miR-210-3p inhibition or ADCY9 overexpression, placing ADCY9 downstream of miR-210-3p in the sevoflurane cardioprotective pathway. |
miR-210-3p agomir/antagomir delivery, ADCY9 overexpression in MI rat model, echocardiography, histology, miRNA-target validation assay |
Functional & integrative genomics |
Low |
34988676
|
| 2023 |
Adcy9 inactivation in mice after myocardial infarction reduces infarct size, pathological left ventricular remodeling, and cardiac dysfunction, and preserves myocardial capillary density in the infarct border zone; increased bone marrow T cells and B cells were also observed. These benefits were only seen in the absence of CETP activity. |
Adcy9Gt/Gt mice, permanent LAD ligation MI model, echocardiography, histology (cardiomyocyte size, infarct size, capillary density), flow cytometry (immune cells) |
The Canadian journal of cardiology |
Medium |
37054880
|
| 2023 |
ADCY9 overexpression in lung adenocarcinoma cell lines (SPCA1, A549) restrains cell proliferation, invasion, and migration, consistent with a tumor-suppressive function mediated through the cAMP pathway. |
ADCY9 overexpression in cancer cell lines, proliferation assay, invasion/migration assays |
Journal of thoracic disease |
Low |
37065546
|
| 2025 |
Asthma-related cytokines decrease ADCY9 expression and cellular cAMP levels in airway smooth muscle cells (ASMCs), reducing airway relaxation and promoting remodeling. ADCY9 overexpression attenuates airway smooth muscle remodeling, but the missense variant ADCY9-Ile772Met (rs2230739) fails to prevent remodeling, demonstrating that the Ile772Met substitution impairs ADCY9's protective function in the airway. |
ADCY9 overexpression and mutant (Ile772Met) expression in ASMCs, cAMP measurement, airway remodeling assays, FEV1/FVC% clinical correlation |
Biochimica et biophysica acta. Molecular basis of disease |
Medium |
40816614
|
| 2027 |
In planarian (Dugesia japonica), ADCY9 knockdown causes abnormal brain regeneration (loss of nerve cord, reduced collateral branches, inhibited neuron regeneration/differentiation). Double RNAi of ADCY9 and Mitofusin-1 restores neural regeneration, indicating ADCY9 promotes neural regeneration by negatively regulating the downstream inhibitory factor Mitofusin-1 in the cAMP/AMPK signaling pathway. |
RNAi knockdown (single and double) in planarians, RNA sequencing, KEGG pathway analysis, morphological assessment of brain regeneration |
Cells |
Low |
41827823
|