| 1999 |
OCNC1 (CNGA2) is required for olfactory signal transduction: knockout mice showed thinner olfactory epithelium with reduced olfactory marker protein and GAP-43 expression, smaller olfactory bulbs, and reduced tyrosine hydroxylase in periglomerular neurons, indicating CNGA2 is essential for normal development and afferent-activity-driven maturation of both olfactory epithelium and olfactory bulb. |
Targeted gene knockout with morphological, biochemical, and immunohistochemical analysis in adult null mice |
The Journal of neuroscience |
High |
10531436
|
| 2001 |
CNGA2-mediated olfactory activity is required for competitive survival of olfactory sensory neurons: in heterozygous females with mosaic X-inactivation, CNGA2-deficient neurons were selectively depleted from the olfactory epithelium upon odorant exposure, and this depletion was reversed by odorant deprivation, demonstrating that evoked activity through CNGA2 is critical for neuronal survival in a competitive environment. |
Reporter-tagged OCNC1 (CNGA2) mutant mice; X-inactivation mosaic analysis; odorant deprivation/exposure experiments with histological readout |
Cell |
High |
11257220
|
| 2006 |
The pore-loop glutamate E342 of CNGA2 is the primary determinant of cation-anion selectivity: point mutation of E342 to lysine or arginine switched the channel from cation-selective (P_Cl/P_Na = 0.07) to anion-selective (P_Cl/P_Na = 14 or 10), demonstrating that the charge of this residue, rather than pore-helix dipoles, controls ion selectivity. |
Site-directed mutagenesis; inside-out patch-clamp with reversal potential measurements and bi-ionic substitution experiments in HEK293 cells expressing rat CNGA2 |
The Journal of general physiology |
High |
16533895
|
| 2005 |
Pore glutamate E342 of CNGA2 controls voltage-dependence, state-dependence, and both cytoplasmic and external dequalinium block: neutralizing E342 (E342Q) drastically reduced voltage-dependence (zdelta from +0.8 to +0.1), abolished state-dependent block (WT prefers closed state; mutant is state-independent), and increased external dequalinium IC50 ~5-fold, placing E342 about two-fifths along the transmembrane electric field as a key pore-lining residue. |
Site-directed mutagenesis (E342Q); inside-out patch-clamp; concentration-response and voltage-dependence analysis of dequalinium block in HEK293 cells expressing rat CNGA2 |
European biophysics journal |
High |
15928936
|
| 2008 |
CNGA2 mediates adenosine-induced Ca2+ influx in vascular endothelial cells via A2B receptors and adenylyl cyclase: adenosine-induced Ca2+ influx and cation current were blocked by CNG channel inhibitors (L-cis-diltiazem, LY-83583) and adenylyl cyclase inhibitors, but not by guanylyl cyclase inhibitor ODQ; CNGA2-specific siRNA markedly reduced both Ca2+ influx and current; L-cis-diltiazem also inhibited NECA-induced vasorelaxation in mouse aortic strips. |
CNGA2-specific siRNA knockdown; patch-clamp; Ca2+ fluorescence imaging; pharmacological inhibitors in H5V endothelial cells, primary bovine aortic endothelial cells, and mouse aortic strips |
Arteriosclerosis, thrombosis, and vascular biology |
Medium |
18292397
|
| 2009 |
CNGA2 contributes to ATP-induced non-capacitative Ca2+ entry in vascular endothelial cells via P2Y1 receptors and adenylyl cyclase: CNG channel inhibitors (L-cis-diltiazem, LY-83583) and CNGA2-specific siRNA reduced ATP-induced non-CCE; the effect was blocked by adenylyl cyclase inhibitors and P2Y1 inhibitor MRS-2179, but not by guanylyl cyclase inhibitor ODQ. |
CNGA2-specific siRNA knockdown; Ca2+ fluorescence imaging; pharmacological inhibitors in H5V cells, primary bovine aortic endothelial cells, and isolated mouse aortic strips |
Journal of vascular research |
Medium |
19729961
|
| 2011 |
CNGA2 channel activity regulates axonal convergence and neuronal survival of olfactory sensory neurons through a feedback loop with retinoic acid metabolism: CNG channel-deficient mice showed defective axonal convergence and increased cell death; retinoic acid receptor inhibition reduced CNG channel expression; CNG channel activity in turn regulated expression of the RA-degrading enzyme Cyp26B1, establishing a homeostatic feedback mechanism. |
CNG channel-deficient (Cnga2) mice; dominant-negative RAR transgenic mice; naris occlusion; immunohistochemistry; gene expression analysis |
FASEB journal |
Medium |
22009938
|
| 2013 |
CNGA2 homotetrameric channels exhibit concentration-dependent gating hysteresis: ligand unbinding is ~50-fold faster at saturating than subsaturating fcGMP concentrations; Markovian modeling revealed two unbinding pathways—partially liganded open channels unbind from closed states only, while fully liganded channels reach a distinct open state from which all four ligands unbind rapidly—resulting in different transition pathways for activation versus deactivation. |
Fluorescent cGMP derivative (fcGMP) binding assay; patch-clamp electrophysiology; complex Markovian kinetic modeling of homotetrameric CNGA2 channels |
Nature communications |
High |
24287615
|
| 2024 |
CNGA2 mediates CIH-induced enhanced Ca2+ influx in carotid body glomus cells downstream of Adcy3-dependent cAMP: CIH-induced glomus cell Ca2+ responses were absent in Cnga2 mutant mice, placing CNGA2 downstream of the Olfr78/H2S/Adcy3/cAMP signaling axis in carotid body activation. |
Cnga2 knockout mice; glomus cell Ca2+ imaging under chronic intermittent hypoxia (CIH) protocol; comparison with Adcy3 and Olfr78 mutants |
bioRxiv (preprint)preprint |
Medium |
bio_10.1101_2024.09.24.614747
|