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the Endoplasmic reticulum calcium sensor protein STIM1 (stromal interaction molecule 1) interacts with the plasma membrane-localized adenylyl cyclase 6 (ADCY6) to govern melanogenesis.
PDE8 is expressed in lipid rafts of human airway smooth muscle cells(HASM), where it specifically regulates beta2-adrenergic receptor/ AC6 signaling to modulate HASM responsiveness and airway remodeling in asthma.
rs3730071G/T and rs77913913G/T of ADCY6 were non-polymorphic with respect to HAPE.
model suggests Cys1004 in AC6 (subunit C2) and Cys174 in Galphas present at the AC-Galphas interface as the possible residues that might undergo reversible nitrosylation. Docking analysis predicted novel ligands of AC6 that include forskolin-based compounds and its derivatives.
Sickle cell anemia patients carrying at least one allele of adcy6 rs3730070-G exhibited lower hemolytic rate than non-carriers in univariate analysis (p=0.006).
LRs are essential not only for the proper membrane distribution and maintenance of AC5/6 activity but also for the regulation of D1R- and D5R-mediated AC signaling.
Mutations in CNTNAP1 and ADCY6 are responsible for severe arthrogryposis multiplex congenita with axoglial defects
AC6 localizes in lipid raft fractions of bronchial airway smooth muscle where it is stimulated by beta2 adrenergic- and prostacyclin receptors and inhibited by divalent calcium ions.
In addition to its direct effect on renin gene transcription, PPARgamma "sensitizes" renin gene to cAMP via trans-activation of AC6 gene.
expression of nodular ADCY6, but not ADCY3, was lower than the expression of both in perinodular tissue, which may be part of the mechanisms occurring in the hyperfunctioning nodules
identified a single nucleotide polymorphism that may play a role in developing left ventricular hypertrophy
Raf1 potentiates drug-stimulated cyclic AMP accumulation in cells expressing adenyl cyclcase 6 after activation of multiple signaling pathways.
A2bR signals through adenylate cyclase (AC) 6 isoform in intestinal epithelial cells
AC6 overexpression in endothelial cells may have use as a means to enhance prostacyclin function and reduce endothelial barrier permeability.
Adenylyl cyclase V and adenylyl cyclase VI interacts with A-kinase anchoring protein 79 (AKAP79) in a complex that associates with protein kinase A forming a negative feedback loop that termporally regulates cAMP production.
These data show that, in an animal model that mimics key aspects of clinical congestive heart failure, cardiac gene transfer of ACVI increases function of the failing heart.
G protein betagamma subunits stimulate type V and VI adenylyl cyclases
Expression of a novel, relatively common variant of ADCY6 parallels an increase in adenylyl cyclase activity and adenylyl cyclase-mediated function in humans.
Parathyroid hormone communicates with IP(3)R via "cAMP junctions" that allow local delivery of a supramaximal concentration of cAMP to IP(3)R, directly increasing their sensitivity to IP(3).
The catalytic domains (C1 and C2) of adenylate cyclase 6 play a role in targeting adenylate cyclase 6 to lipid rafts.
Instead the knock down of the predominant subtype AC6 in HUVECs provided the first direct evidence that the Ca(2+)-mediated inhibition of AC6 accounts for the thrombin-induced decrease in cAMP levels.
Under baseline conditions, renal adenylate cyclase 6 (AC6) is redundant for acid-base balance but becomes important under alkaline conditions.
AC6 has a minor role in lithium-induced nephrogenic diabetes insipidus development but may be important for determining the intercalated cell-to-principal cell ratio.
Immunofluorescence staining revealed that cardiac AC6 was mainly anchored on the sarcolemmal membranes, while AC6-DeltaN was redistributed to the sarcoplasmic reticulum. AC6(DeltaN/DeltaN) and AC6(-/-) mice had more apoptotic myocytes and cardiac remodeling than WT mice in experimental models of isoproterenol (ISO)-induced myocardial injury.
GluN2B-dependent calcium signaling and excitatory postsynaptic current, long-term depression, and spatial reversal learning are enhanced in the hippocampus of AC6(-/-) mice without altering the gross anatomy of the brain
Expression level of AC6 is positively associated with HSF1 in heart failure.
The role of AC6 in beta-adrenoceptor signalling in murine airways
Pkd1(RC/RC) mice experience hepatic hypertrophy that can be corrected by pasireotide through a pathway involving AC6 and cAMP
AC6 in the proximal tubule modulates cAMP formation, Npt2a trafficking, and urinary phosphate excretion, which are highlighted by renal phosphate wasting in AC6(-/-) mice
Cytokine-induced iNOS and ERK1/2 inhibit adenylyl cyclase type 5/6 activity and stimulate phosphodiesterase 4D5 activity in intestinal longitudinal smooth muscle, contributing to colonic dysmotility during inflammation.
data indicate that AC6 plays a role in loading-induced bone adaptation, and these findings are consistent with our previous studies implicating primary cilia and AC6 in a novel mechanism of osteocyte mechanotransduction
AC6 is a key mediator of cyst formation and renal injury in a model of PKD.
Adenylyl cyclase 6 mediates the action of cyclic AMP-dependent secretagogues in mouse pancreatic exocrine cells via protein kinase A pathway activation.
AC6 plays a key role in negative regulation of TLR4 signaling by promoting protein degradation. AC6 activation shifts TLR4 to lipid raft-mediated endocytosis, accelerating its degradation & suppressing downstream signaling.
AC6 deletion impairs electrophysiological properties and increases mortality during sustained beta-adrenergic receptor stimulation.
AC6 plays a critical role in the regulation of sympathetic tone.
ACVI isoform is localized in the plasma membrane outside the t-tubular region and is responsible for beta1-adrenergic receptor signaling-mediated enhancement of the L-type Ca(2+) current in ventricular myocytes.
Adenylyl cyclase 6 enhances NKCC2 expression and mediates vasopressin-induced phosphorylation of NKCC2 and NCC.
These data suggest that adenylyl cyclase VI mediates vasopressin-stimulated ENaC activity in the kidney.
AC6 in the collecting duct regulates renal water excretion, most likely through control of AVP-stimulated cAMP accumulation and AQP2.
In primary hippocampal neurons and Neuro2A cells, elevated AC6 expression suppressed neurite outgrowth, whereas the downregulation or genetic removal of AC6 promoted neurite extension.
co-localization of multiple signaling components in lipid rafts provides key spatial regulation of AC6 (ADCY6) activity.
This gene encodes adenylate cyclase 6, which is a membrane-associated enzyme and catalyzes the formation of the secondary messenger cyclic adenosine monophosphate (cAMP). The expression of this gene is found in normal thyroid and brain tissues, as well as some tumors\; and its expression is significantly higher in one hyperfunctioning thyroid tumor than in normal thyroid tissue. Alternative splicing generates 2 transcript variants.
adenylate cyclase 6
, adenylate cyclase type VI
, adenylyl cyclase type VI
, adenylate cyclase 6-like
, adenylate cyclase type 6-like
, ATP pyrophosphate-lyase 6
, adenylate cyclase type 6
, adenylyl cyclase 6
, ca(2+)-inhibitable adenylyl cyclase