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Regulation of NMDA receptors by an associated phosphatase-kinase signaling complex.
Yotiao is a scaffold protein that physically attaches PP1 and PKA to NMDA receptors to regulate channel activity and targeting of these enzymes near the substrate is proposed to enhance phosphorylation-dependent modulation.
Selective activation of Ca2+-activated K+ channels by co-localized Ca2+ channels in hippocampal neurons
Channel activity in cell-attached patches from hippocampal neurons is studied and a unique specificity of coupling is reported, indicating an absolute segregation of coupling between channels, and illustrating the functional importance of submembrane calcium microdomains.
Regulation of GluR1 by the A-Kinase Anchoring Protein 79 (AKAP79) Signaling Complex Shares Properties with Long-Term Depression
- S. J. Tavalin, M. Colledge, J. Hell, L. Langeberg, R. Huganir, John D. Scott
- BiologyThe Journal of Neuroscience
- 15 April 2002
It is demonstrated that AKAP79 not only promotes basal phosphorylation of Ser845 but also confers a calcium- and PP2B-mediated downregulation to GluR1 receptor currents, suggesting that the integration of intracellular signals relevant for LTD may be transduced to GLUR1 by theAKAP79 signaling complex.
A novel lipid‐anchored A‐kinase Anchoring Protein facilitates cAMP‐responsive membrane events
Cloned a low‐molecular weight A‐kinase Anchoring Protein, called AKAP18, is cloned, which targets the cAMP‐dependent protein kinase (PKA) to the plasma membrane, and permits functional coupling to the L‐type calcium channel, and facilitates GLP‐1‐mediated insulin secretion in a pancreatic β cell line.
Endocytosis and synaptic removal of NR3A-containing NMDA receptors by PACSIN1/syndapin1
It is demonstrated that NMDARs containing the developmentally regulated NR3A subunit undergo rapid endocytosis from the dendritic plasma membrane in cultured rat hippocampal neurons, and a brain-specific endocytic adaptor is identified that confers spatiotemporal and subunit specificity to N MDAR endocyTosis.
Mapping the Protein Phosphatase-2B Anchoring Site on AKAP79
- M. Dell'Acqua, K. Dodge, S. J. Tavalin, John D. Scott
- Biology, ChemistryThe Journal of Biological Chemistry
- 13 December 2002
It is demonstrated that residues 315–360 are necessary and sufficient for AKAP79-PP2B anchoring in cells and proposed that the structural features of this AKAP 79-PP 2B-binding domain may share similarities with other proteins that serve to coordinate PP2B localization and activity.
AKAP79 Selectively Enhances Protein Kinase C Regulation of GluR1 at a Ca2+-Calmodulin-dependent Protein Kinase II/Protein Kinase C Site*
- S. J. Tavalin
- Biology, ChemistryJournal of Biological Chemistry
- 25 April 2008
Biochemical studies demonstrate that AKAP79 localizes PKC activity near the receptor, thus accelerating Ser-831 phosphorylation, and provides a mechanism to overcome limitations in kinase abundance thereby ensuring faithful signal propagation and efficient modification of AMPA receptor-mediated responses.
Contribution of L- and non-L-type calcium channels to voltage-gated calcium current and glucose-dependent insulin secretion in HIT-T15 cells.
The pharmacological properties of voltage-gated Ca current and glucose-dependent insulin secretion were determined using the HIT insulinoma line to understand the role of Ca channels in stimulus-secretion coupling and suggest that persistent Ca current is mediated by L-channels and is strongly coupled to insulin secretion, whereas transient CaCurrent is mediatedBy L- and N-ch channels and is weakly coupled.
Mechanical perturbation of cultured cortical neurons reveals a stretch-induced delayed depolarization.
Stretch-induced delayed depolarization was dependent on the degree of cell stretch and required neuronal firing, calcium entry, and N-methyl-D-aspartate receptor activation for its induction but not its maintainance, suggesting that SIDD may play a role in brain injury.
Inhibition of the electrogenic Na pump underlies delayed depolarization of cortical neurons after mechanical injury or glutamate.
It is reported that SIDD is mediated by Na pump inhibition and is likely to result from reduced energy levels since the RMP of neurons dialyzed with a pipette solution containing 5 mM ATP were identical to controls.