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These findings suggest that AKAP79, by orchestrating phosphorylation, represents a key to a GluA1 phosphorylation passcode, which allows the GluA1 subunit to escape GluA2 dominance and promote the appearance of CP-AMPARs.
results provide the first direct evidence for a function of the well-described AKAP79/150 trafficking in regulating LTD-induced spine shrinkage.
We determined a crystal structure of CaM bound to a peptide encompassing its binding site in AKAP79. CaM adopts a highly compact conformation in which its open Ca(2+)-activated C-lobe and closed N-lobe cooperate to recognize a mixed alpha/310 helix in AKAP79.
A short-linear interaction motif between residues 337-343 of AKAP79 is the sole PP2B-anchoring determinant sustaining these diverse topologies.
Studies indicate the importance of the AKAP79/PP2B/protein kinase A complex's role in synaptic long-term depression in the CA1 region of the hippocampus.
Cigarette smoke-induced changes in AKAP5 and AKAP12 in patients with COPD may affect efficacy of pharmacotherapy.
human AKAP79-anchored PKC selectively phosphorylates the Robo3.1 receptor subtype on serine 1330
GPR30 interacted with membrane-associated guanylate kinases and protein kinase A-anchoring protein (AKAP) 5 in the plasma membrane in a PDZ-dependent manner.
a significant role for the AKAP5 scaffold in signaling and trafficking of the beta1-AR in cardiac myocytes and mammalian cells.
Patients with bipolar disorder have higher density of AKAP5-expressing neurons in the anterior cingulate cortex compared with controls.
AKAP79, PKC, PKA and PDE4 participate in a Gq-linked muscarinic receptor and adenylate cyclase 2 cAMP signalling complex.
The results of this study suggested that antagonizing the TRPV1-AKAP79 interaction will be a useful strategy for inhibiting inflammatory hyperalgesia.
AKAP5 Pro100Leu effects on emotion processing might be task-dependent with Pro homozygotes showing lower control of emotional interference, but more efficient processing of task-relevant emotional stimuli.
Antagonizing the interaction between AKAP79 and TRPV1 inhibits inflammatory hyperalgesia.
the direct anchoring of both PKA and AC to TRPV1 by AKAP79/150 facilitates the response to inflammatory mediators and may be critical in the pathogenesis of thermal hyperalgesia.
AKAP79 directly interacts with Cav1.2 c-terminus and modulates Cav1.2 membrane targeting.
We demonstrate that calmodulin and caldendrin compete for a partially overlapping binding site on AKAP79 and that their binding is differentially dependent on calcium
results reveal novel roles for the AKAP79/150 signaling complex in dendritic endosomes.
show that an IAIIIT anchoring site in human AKAP79 binds the same surface of calcineurin as the PxIxIT recognition peptide of NFAT, albeit more strongly
Mutation of the two critical cysteines results in exclusion of AKAP79 from lipid rafts and alterations in its membrane diffusion behavior and is accompanied by a loss of the ability of AKAP79 to regulate AC8.
the C-helix of protein kinase A inhibitory regulatory subunit is identified as a highly dynamic switch which relays cyclic AMP binding to the helical catalytic-subunit binding regions
AKAP150 regulates Ca(2+ )cycling and myocardial ionotropy following pathological stress, promoting pathological remodelling and heart failure propensity.
AKAP150-calcineurin signaling dyad is essential for the activation of the phosphatase and the subsequent down-regulation of Kv channel currents following myocardial infarction.
This study demonstrated that the AKAP150 oordinates metabotropic glutamate receptor sensitization of peripheral sensory neurons.
Thus, our present study revealed that AKAP5 plays a significant role in the regulation of sympathetic nerve activities.
Identify a novel cardioprotective role for AKAP5 that is mediated by regulating the activities of cardiac CaN and CaMKII and highlight a significant role for cardiac beta-ARs in this phenomenon.
endothelial-dependent dilation of resistance arteries is enabled by MEP-localized AKAP150, which ensures the proximity of PKC to TRPV4 channels and the coupled channel gating necessary for efficient communication from endothelial to smooth muscle cells
Our results support a model whereby subcellular anchoring of CaN by AKAP150 is a key molecular determinant of vascular BKCa channel remodeling, which contributes to vasoconstriction during diabetes mellitus.
Anchoring of protein kinase A and adenylyl cyclase by AKAP5 is important for regulation of postsynaptic functions and specifically AMPA receptor activity.
Results show that in the same protein complex in which PKA augments L currents, AKAP79/150 directs calcineurin to activate NFAT and initiate a longer-term feedback loop that upregulates M-channel expression, countering increased neuronal excitability.
AKAP150 null mice secrete less insulin yet have better glucose handling due to increased insulin sensitivity in target tissues. Tethering of phosphatases to a seven-residue sequence of Akap5 is the main molecular event for this.
This study demonistrated taht AKAP79/150-anchored CaN in regulation of Ca2+-permeable GluA1 homomers that our results here now clearly establish as a key mechanism that maintains bidirectional synaptic plasticity in the hippocampus.
A kinase anchor protein 150 (AKAP150)-associated protein kinase A limits dendritic spine density
We propose that AKAP150-dependent changes in Ca(V)1.2-LQT8 channel gating may constitute a novel general mechanism for Ca(V)1.2-driven arrhythmias.
other neural AKAPs cannot compensate for the loss of PKA binding to AKAP5
In knockout AKAP5 cardiomyocytes, beta-adrenergic regulation of calcium transients is disrupted.
Study reveals that non-neurotransmitter Abeta has a binding capacity to beta(2)AR and induces PKA-dependent hyperactivity in AMPA receptors.
These data suggest that isoproterenol-stimulated amylase secretion occurs via both an AKAP5/AC6/PKA complex and a PKA-independent, Epac pathway in mouse parotid acini.
An important role of AKAP150 in coordinating signaling events regulating the frequency of intrinsic pulsatile GnRH secretion.
The A-kinase anchor proteins (AKAPs) are a group of structurally diverse proteins, which have the common function of binding to the regulatory subunit of protein kinase A (PKA) and confining the holoenzyme to discrete locations within the cell. This gene encodes a member of the AKAP family. The encoded protein binds to the RII-beta regulatory subunit of PKA, and also to protein kinase C and the phosphatase calcineurin. It is predominantly expressed in cerebral cortex and may anchor the PKA protein at postsynaptic densities (PSD) and be involved in the regulation of postsynaptic events. It is also expressed in T lymphocytes and may function to inhibit interleukin-2 transcription by disrupting calcineurin-dependent dephosphorylation of NFAT.
A kinase (PRKA) anchor protein 5
, A-kinase anchor protein 5
, A-kinase anchor protein 5-like
, a-kinase anchor protein 5-like
, A-kinase anchor protein 79 kDa
, A-kinase anchor protein, 79kDa
, A-kinase anchoring protein 75/79
, AKAP 79
, cAMP-dependent protein kinase regulatory subunit II high affinity binding protein
, cAMP-dependent protein kinase regulatory subunit II high affinity-binding protein
, A-kinase anchor protein 75 kDa
, AKAP 75
, anchor protein regulatory subunit (AKAP75)
, A-kinase anchor protein 150 kDa
, AKAP 150
, RII-B-binding protein