-
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.
-
AKAP79 may be the key AKAPs responsible for regulating antigen presentation.
