Affinage

AKAP5

A-kinase anchor protein 5 · UniProt P24588

Length
427 aa
Mass
47.1 kDa
Annotated
2026-04-28
91 papers in source corpus 51 papers cited in narrative 50 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

AKAP5 (AKAP79 in human, AKAP150 in rodents) is a multivalent scaffold protein that orchestrates bidirectional phospho-signaling at the plasma membrane by simultaneously anchoring PKA, calcineurin (PP2B), PKC, PP1, and adenylyl cyclases (AC5/6/8/9) through distinct, mapped binding domains, thereby coordinating the phosphorylation state of ion channels, receptors, and transcription factors in neurons, cardiomyocytes, smooth muscle, and pancreatic β-cells (PMID:8599116, PMID:21561082, PMID:20231277). Membrane targeting depends on three N-terminal polybasic regions that bind PIP2, with dynamic regulation by palmitoylation (via DHHC2), Ca²⁺/calmodulin displacement, and CaMKII phosphorylation controlling stimulus-selective trafficking into and out of dendritic spines during LTP and LTD (PMID:9545238, PMID:25589740, PMID:29196604). The scaffold assembles as a dimer that positions PKA-RII and calcineurin within ~50 Å, enabling calcineurin to accelerate RII dephosphorylation ~10-fold and thereby suppress PKA without changing cAMP, while PKC anchored to the same complex phosphorylates substrates such as GluA1 Ser831 and KCNQ2 to control AMPA receptor calcium permeability and M-channel excitability (PMID:12507994, PMID:34612814, PMID:20188672, PMID:30737285). AKAP5 also recruits NFAT via a C-terminal leucine zipper and couples local Ca²⁺ entry through CaV1.2 and Orai1 to calcineurin-dependent NFAT nuclear translocation, linking channel activity to gene expression programs including activity-dependent KCNQ2/3 upregulation (PMID:31091162, PMID:33941685, PMID:23259949).

Mechanistic history

Synthesis pass · year-by-year structured walk · 24 steps
  1. 1993 High

    Identification of the membrane-targeting and PKA-RII-binding domains established that AKAP5 uses physically separable determinants for subcellular localization versus kinase anchoring.

    Evidence Deletion and scanning mutagenesis of bovine AKAP75 in HEK293 cells with RII overlay assay

    PMID:8509414

    Open questions at the time
    • Lipid specificity of membrane-targeting domains not yet defined
    • Structure of the RII-binding helix not resolved
  2. 1996 High

    Demonstration that a single scaffold simultaneously binds PKA, calcineurin, and PKC at distinct sites established the multivalent signaling-hub concept for AKAPs.

    Evidence Deletion analysis, co-immunoprecipitation, and immunofluorescence in hippocampal neurons

    PMID:8599116

    Open questions at the time
    • Stoichiometry of multi-enzyme assembly unknown
    • Functional consequences for substrates not yet tested
  3. 1997 High

    Discovery that Ca²⁺/calmodulin competes with PKC for the same N-terminal AKAP79 region revealed a Ca²⁺-dependent switch controlling which enzyme occupies the scaffold.

    Evidence Calmodulin binding assays and PKC activity assays from postsynaptic density preparations

    PMID:9202019

    Open questions at the time
    • In vivo dynamics of CaM/PKC competition not measured
    • Whether CaM displaces PKC during synaptic activity unknown
  4. 1998 High

    Mapping PIP2-dependent membrane anchoring to three polybasic N-terminal regions and showing their disruption by phosphorylation and Ca²⁺/CaM established a regulated membrane-release mechanism for the scaffold.

    Evidence GFP targeting assays, lipid vesicle binding, subcellular fractionation in HEK293 and cortical neurons

    PMID:9545238

    Open questions at the time
    • Identity of palmitoylating enzyme unknown at this time
    • Whether membrane release occurs during synaptic plasticity not shown
  5. 1999 High

    Elucidation that AKAP79 inhibits PKC by displacing its pseudosubstrate domain via R39/R40 contacts explained how the scaffold holds PKC in an inactive-but-releasable state.

    Evidence In vitro kinase assays, limited proteolysis, and site-directed mutagenesis with multiple PKC isoforms

    PMID:10510312

    Open questions at the time
    • Structural basis of pseudosubstrate displacement not resolved
    • Release kinetics in cells unknown
  6. 2002 High

    A series of studies established that AKAP79 connects to AMPA receptors via SAP97 to mediate PKA-dependent GluA1 Ser845 phosphorylation and calcineurin-dependent current rundown, providing a molecular mechanism for bidirectional synaptic plasticity and a direct role in LTD-like processes.

    Evidence Co-immunoprecipitation, electrophysiology in HEK293 and hippocampal neurons, FRET microscopy showing PKA-RII and calcineurin within ~50 Å on the scaffold

    PMID:11943807 PMID:12354762 PMID:12507994

    Open questions at the time
    • Whether this complex operates at single identified synapses in vivo not shown
    • Relative contribution of PP2B versus PP1 in LTD unclear
  7. 2002 High

    Demonstration that AKAP79 controls CaV1.2 surface expression via the channel's II–III loop polyproline motif revealed a PKA-independent scaffolding function for channel trafficking.

    Evidence Extracellular epitope tagging, single-channel and whole-cell electrophysiology

    PMID:12114507

    Open questions at the time
    • Mechanism by which AKAP79 relieves autoinhibition of CaV1.2 not fully resolved
    • In vivo cardiac consequences not tested at this point
  8. 2005 High

    Identification of AKAP79 as the specific AKAP that provides PKA for β2-AR Gs-to-Gi switching, opposed by PDE4D5/β-arrestin, placed AKAP5 at the center of GPCR signaling bias.

    Evidence Isoform-selective siRNA, PKA activity assays, ERK phosphorylation in HEK293B2 cells

    PMID:16030021

    Open questions at the time
    • Whether this mechanism operates in cardiomyocytes or neurons not tested
    • Direct structural interface between AKAP79 and β2-AR not mapped
  9. 2006 High

    Showing that AKAP79–SAP97 forms a receptosome with β1-AR where PKA phosphorylation at Ser312 dictates recycling defined the scaffold's role in receptor resensitization.

    Evidence siRNA, FRET, receptor recycling assays, PDZ motif mutagenesis in HEK293 and SK-N-MC cells

    PMID:16940053 PMID:17170109

    Open questions at the time
    • Whether recycling pathway is conserved across all β1-AR-expressing tissues unknown
  10. 2007 High

    Co-targeting of PKA and calcineurin to CaV1.2 by AKAP79/150 was shown to produce bidirectional L-type current regulation with dominant calcineurin suppression, and to couple local Ca²⁺ entry to NFAT activation—linking channel regulation to gene expression.

    Evidence Co-immunoprecipitation, electrophysiology in HEK293 and hippocampal neurons, NFAT reporter assays

    PMID:17640527

    Open questions at the time
    • Whether NFAT isoform selectivity exists in this complex not addressed
    • Distance constraints between channel pore and calcineurin active site unknown
  11. 2008 High

    Mapping the AKAP79–TRPV1 interaction to the TRPV1 C-terminus and demonstrating that the complex mediates inflammatory heat hyperalgesia in vivo extended the scaffold's role to nociception.

    Evidence Deletion mapping, electrophysiology, in vivo hyperalgesia assays

    PMID:18701070

    Open questions at the time
    • Structural basis of TRPV1–AKAP79 binding not resolved
    • Contribution of individual enzymes (PKA vs PKC vs calcineurin) to sensitization not fully parsed
  12. 2010 High

    Multiple 2010 studies collectively established that AKAP5 anchors adenylyl cyclases (AC5/6/8/9) via residues 77–108, organizes them in caveolin-3 complexes in cardiomyocytes for β-adrenergic calcium transients, limits AC8 Ca²⁺ sensitivity, and anchors PKC to KCNQ2 M-channels—demonstrating the scaffold coordinates both cAMP production and ion channel modulation.

    Evidence AKAP5 KO mice, FRET in living cells, calcium imaging, electrophysiology, AC activity assays in brain extracts

    PMID:20147557 PMID:20188672 PMID:20231277 PMID:20410303 PMID:20671242

    Open questions at the time
    • Whether AC isoform selectivity differs between cell types not resolved
    • Structural basis for AC N-terminal interaction with AKAP79 unknown
  13. 2010 High

    Genetic dissection using AKAP5 KO versus D36 (PKA-binding-deleted) knock-in mice proved that PKA anchoring by AKAP5 is specifically required for postsynaptic PKA localization, synaptic plasticity, and operant learning.

    Evidence KO and domain-deletion knock-in mice, electrophysiology, immunofluorescence, behavioral assays

    PMID:20428246

    Open questions at the time
    • Relative contribution of calcineurin-anchoring versus PKA-anchoring to learning not separated in this study
  14. 2011 High

    Native mass spectrometry revealed AKAP79 dimerizes and assembles a 466-kDa complex with defined stoichiometry (2 AKAP79 : 2 RII dimers : 4 PP2B heterodimers : 2 CaM), where Ca²⁺/CaM generates a second PP2B interface to activate anchored phosphatase.

    Evidence Native mass spectrometry, chemical cross-linking, quantitative reconstitution

    PMID:21464287

    Open questions at the time
    • How dimerization interfaces relate to substrate access unknown
    • Whether dimeric vs monomeric forms differ in cellular context not tested
  15. 2011 High

    Identification of N-terminal palmitoylation sites as required for lipid-raft targeting, AC8 regulation, and raft-associated PKA signaling established lipid modification as a major determinant of scaffold compartmentalization.

    Evidence Palmitoylation-site mutagenesis, FRAP, lipid-raft fractionation, AC activity assays in HEK293 cells

    PMID:21771783

    Open questions at the time
    • Identity of palmitoyl acyltransferase not determined at this stage
  16. 2012 High

    The calcineurin-anchoring motif IAIIIT (residues 337–343) was shown to occupy the same PxIxIT surface on calcineurin as NFAT, establishing an optimal-affinity window where too-tight AKAP–calcineurin binding sequesters calcineurin away from NFAT substrates.

    Evidence Structural analysis, mutagenesis of anchoring sequence, NFAT reporter assays in hippocampal neurons

    PMID:22343722

    Open questions at the time
    • Full atomic-resolution structure of AKAP79–calcineurin complex not available
    • Whether affinity tuning is dynamically regulated in vivo unknown
  17. 2012 High

    AKAP79/150–calcineurin–NFAT signaling was shown to drive activity-dependent transcriptional upregulation of KCNQ2/3 after seizures, requiring L-type Ca²⁺ influx and absent in AKAP150 KO mice, establishing a gene-expression feedback loop from channel to scaffold to transcription.

    Evidence AKAP150 KO mice, in vivo seizure induction, KCNQ2/3 mRNA quantification, NFAT reporter assays

    PMID:23259949

    Open questions at the time
    • Full set of NFAT target genes regulated by AKAP150 not identified
    • Whether this loop operates in non-seizure physiological activity unknown
  18. 2015 High

    Identification of DHHC2 as the palmitoyl acyltransferase that palmitoylates AKAP79/150 on recycling endosomes, and demonstration that this is required for LTP-induced spine delivery and AMPAR potentiation, completed the palmitoylation-dependent trafficking mechanism.

    Evidence RNAi knockdown, palmitoylation assay, exocytosis assay, spine morphology, AMPAR recordings, rescue with lipidated AKAP mutant

    PMID:25589740

    Open questions at the time
    • Whether depalmitoylation during LTD uses a specific thioesterase not identified
    • Kinetics of palmitoylation cycling at single spines unknown
  19. 2017 High

    Negative-stain EM and mutagenesis revealed that intrinsic disorder in AKAP79 allows an ensemble of configurations with calcineurin; Ca²⁺/CaM engagement of additional motifs (including LKIP at residues 125–128) condenses the ensemble, fine-tuning phosphatase activity and drug sensitivity.

    Evidence Negative-stain EM, chemical cross-linking, NFAT translocation reporters, mutagenesis

    PMID:28967377

    Open questions at the time
    • High-resolution structure of the full-length complex still lacking
    • How ensemble condensation changes substrate selectivity in cells not measured
  20. 2017 High

    CaMKII was shown to drive LTD-associated synaptic removal of AKAP79/150 by promoting depalmitoylation and phosphorylating the N-terminal polybasic domain to inhibit F-actin binding, with Ca²⁺/CaM protecting these sites during LTP-type stimuli—explaining stimulus-selective scaffold trafficking.

    Evidence CaMKII inhibitors/KO, LTD induction, palmitoylation assay, actin-binding assay, phospho-site mutagenesis in hippocampal neurons

    PMID:29196604

    Open questions at the time
    • Specific CaMKII phospho-sites on AKAP150 not all mapped
    • Whether CaM protection is quantitatively sufficient in all stimulus regimes unclear
  21. 2019 High

    Demonstration that AKAP79 recruits NFAT via a C-terminal leucine zipper (rather than through the LTCC interaction alone) resolved how the scaffold pre-positions NFAT near local Ca²⁺ sources for excitation–transcription coupling.

    Evidence LZ-deletion mutant replacement, co-IP, FRET, Ca²⁺ imaging, FCS in hippocampal neurons

    PMID:31091162

    Open questions at the time
    • Whether the LZ domain recruits other transcription factors not tested
    • Structural basis of AKAP79 LZ–NFAT interaction not resolved
  22. 2020 High

    AKAP5 was shown to organize a P2Y11–AC5–PKA–CaV1.2 nanocomplex in arterial myocytes required for glucose-induced vasoconstriction, extending the scaffold's physiological roles to vascular tone regulation.

    Evidence AKAP5 KO mice, proximity ligation assay, TIRF, patch-clamp, myography

    PMID:33082339

    Open questions at the time
    • Whether this complex is altered in diabetes not tested
    • Precise stoichiometry in vascular smooth muscle unknown
  23. 2021 High

    NMR structural analysis of the Orai1 N-terminus revealed a compact proline-driven structure mediating AKAP79 binding that is unique to full-length Orai1, and disrupting this interface suppressed NFAT-dependent cytokine production without affecting other Orai1 functions—establishing a selective excitation–transcription coupling mechanism.

    Evidence NMR, co-IP, NFAT translocation, cytokine assay, Orai isoform comparison

    PMID:33941685

    Open questions at the time
    • Whether pharmacological disruption of Orai1–AKAP79 is therapeutically viable not tested
    • Full interface structure at atomic resolution not available
  24. 2021 High

    Reconstitution showed AKAP79 accelerates calcineurin-mediated RII dephosphorylation ~10-fold, enabling calcineurin to suppress PKA activity without changing cAMP—establishing a cAMP-independent mechanism for PKA inhibition during LTD.

    Evidence In vitro phosphatase assay, fluorescent PKA activity reporter, kinetic modeling, hippocampal neuron electrophysiology

    PMID:34612814

    Open questions at the time
    • Whether this mechanism contributes to non-neuronal AKAP5 functions not tested
    • Relative importance versus direct catalytic subunit inhibition not quantified in vivo

Open questions

Synthesis pass · forward-looking unresolved questions
  • High-resolution structural determination of the full-length AKAP79 dimer in complex with its enzyme cohort, and understanding how the intrinsically disordered scaffold selects among multiple substrates in a stimulus-specific manner, remain unresolved.
  • No atomic-resolution structure of full-length AKAP79 or its multi-enzyme complexes
  • Mechanisms governing substrate selectivity among co-anchored enzymes in physiological settings largely inferred from reconstitution
  • Whether AKAP5 mutations contribute to human neurological or cardiovascular disease not established

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 4 GO:0060090 molecular adaptor activity 3 GO:0008289 lipid binding 1
Localization
GO:0005886 plasma membrane 5 GO:0031410 cytoplasmic vesicle 1
Pathway
R-HSA-112316 Neuronal System 5 R-HSA-162582 Signal Transduction 5 R-HSA-382551 Transport of small molecules 4 R-HSA-74160 Gene expression (Transcription) 4
Partners
ADCY5ADCY8CACNA1CDLG1ORAI1PPP3CAPRKAR2ATRPV1
Complex memberships
AKAP79–AC5/6/8–PKA signalosomeAKAP79–CaV1.2–PKA–calcineurin complexAKAP79–PKA-RII–calcineurin ternary complexAKAP79–SAP97–GluA1 complex

Evidence

Reading pass · 50 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1996 AKAP79 functions as a scaffold protein that simultaneously binds PKA, calcineurin (PP2B), and PKC at distinct sites, coordinating three signaling enzymes at the postsynaptic membrane. Deletion analysis, binding studies, co-immunoprecipitation, immunofluorescence in neurons Science High 8599116
1993 AKAP75 (bovine ortholog of AKAP5) contains two noncontiguous N-terminal domains (residues 27–48 and 77–91) that mediate intracellular membrane targeting, and a separate C-terminal RII-binding (tethering) domain mapped to residues 392–413 via scanning mutagenesis, where hydrophobic residues are essential for high-affinity PKA-RII binding. Deletion mutagenesis, scanning mutagenesis, subcellular fractionation, RII overlay assay in HEK293 cells The Journal of biological chemistry High 8509414
1997 Ca²⁺/calmodulin binds AKAP79 at the same N-terminal region (residues 31–52) that binds PKC, competing with PKC for binding and releasing the inhibited kinase from the anchoring protein; calmodulin binding also reverses AKAP79-mediated inhibition of PKCβII. Calmodulin binding assays, co-immunoprecipitation from postsynaptic density preparations, immunofluorescence in hippocampal neurons, PKC activity assays The Journal of biological chemistry High 9202019
1998 AKAP79 membrane targeting is mediated by three basic/hydrophobic N-terminal regions (A: residues 31–52; B: 76–101; C: 116–145) that bind acidic phospholipids including PIP2; this binding is disrupted by phosphorylation and Ca²⁺/calmodulin, providing a regulatory mechanism for membrane release. GFP-tagging and in situ fluorescence targeting assays in HEK293 cells and cortical neurons, lipid vesicle binding assays, subcellular fractionation after PKA/PKC activation The EMBO journal High 9545238
1998 AKAP79 binds calcineurin A (CnA) at residues 30–98 and 311–336 of CnA, with the AKAP79 binding site on residues 108–280; this interaction does not require the calcineurin B subunit, occurs at a site distinct from immunophilin binding, and AKAP79 inhibits NFAT dephosphorylation and activation in intact cells. Co-immunoprecipitation, deletion mapping, NFAT reporter assay in transfected cells The Journal of biological chemistry High 9765270
1999 AKAP79 binds PKC at the catalytic core through the N-terminal region (residues 31–52) in a lipid- and activation-independent manner, inhibiting PKC activity by displacing the pseudosubstrate domain; residues R39 and R40 in the AKAP79(31–52) peptide are essential for PKC inhibition. AKAP79 associates with conventional, novel, and atypical PKC isoforms. In vitro binding and kinase activity assays, limited proteolysis, site-directed mutagenesis, co-immunoprecipitation, immunofluorescence in hippocampal neurons The Biochemical journal High 10510312
2001 AKAP79 regulates GRK2-mediated phosphorylation of the β2-adrenergic receptor by facilitating PKA phosphorylation of GRK2 at Ser685, which increases Gβγ binding to GRK2 and promotes its membrane translocation and receptor phosphorylation; disruption of this pathway reduces receptor internalization. Overexpression/dominant-negative approaches, mutagenesis (GRK2 S685A), co-immunoprecipitation, receptor internalization assays in HEK293 cells The Journal of biological chemistry High 11278469
2001 AKAP79 directly associates with the inwardly rectifying potassium channel Kir2.1 via both the intracellular N- and C-terminal domains of the channel, and this association enhances Kir2.1 responsiveness to elevated intracellular cAMP. Co-immunoprecipitation, GST pulldown, electrophysiology in intact cells The Journal of biological chemistry Medium 11287423
2002 The PP2B/calcineurin-anchoring site on AKAP79 maps to residues 315–360, which are necessary and sufficient for PP2B anchoring in cells, directly bind the PP2B A subunit, and inhibit phosphatase activity; peptides spanning this region antagonize PP2B anchoring and attenuate PP2B-dependent down-regulation of GluR1 currents. Deletion/truncation mutagenesis, cell targeting assays, in vitro phosphatase activity assays, peptide competition, electrophysiology in HEK293 cells The Journal of biological chemistry High 12354762
2002 AKAP79 directly regulates cell surface expression (trafficking) of L-type CaV1.2 calcium channels independently of PKA, through interaction involving a short polyproline sequence in the channel II–III cytoplasmic loop. Extracellular epitope tagging, immunoassays, whole-cell and single-channel electrophysiology The Journal of biological chemistry High 12114507
2002 AKAP79 is linked to GluR1 AMPA receptors via SAP97, promoting basal PKA-dependent phosphorylation of GluR1 Ser845, and the AKAP79–PP2B complex confers Ca²⁺-dependent downregulation of GluR1 currents mimicking LTD; this requires the PDZ interaction between GluR1 and SAP97. Co-immunoprecipitation, electrophysiology in HEK293 cells and hippocampal neurons, mutagenesis The Journal of neuroscience High 11943807
2002 AKAP79 assembles a ternary kinase-scaffold-phosphatase complex at the plasma membrane, where PKA-RII and calcineurin bind simultaneously to AKAP79 within ~50 Å of each other, as demonstrated by FRET in living cells; AKAP79 also regulates membrane localization of SAP97. FRET microscopy (donor-dequenching and sensitized emission), immunofluorescence in living cells The Journal of cell biology High 12507994
2003 AKAP79 interacts with IQGAP1 through the carboxyl-terminal domain of IQGAP1, forming a complex that links PKA to the IQGAP1 scaffold in β-cells. cAMP affinity chromatography co-purification, co-immunoprecipitation, direct interaction assay Journal of cellular biochemistry Medium 12938160
2005 AKAP79 (constitutively associated with β2-AR) provides the PKA that mediates β2-AR phosphorylation enabling switching of β2-AR signaling from Gs to Gi/ERK activation; PDE4D5 recruited by β-arrestin desensitizes this PKA-mediated switch. siRNA knockdown of specific AKAPs and PDE4 isoforms, co-immunoprecipitation, PKA activity assays, ERK phosphorylation assays in HEK293B2 cells The Journal of biological chemistry High 16030021
2006 AKAP79 forms a ternary complex with β1-adrenergic receptor and PKA at the receptor C-terminus, and AKAP79-anchored PKA phosphorylates β1-AR at Ser312 (third intracellular loop) to dictate recycling and resensitization itineraries of the internalized receptor. siRNA knockdown, co-immunoprecipitation, FRET microscopy, receptor recycling assays in HEK293 and SK-N-MC cells The Journal of biological chemistry High 16940053
2006 AKAP79 forms a receptosome with SAP97 at the type I PDZ motif (ESKV) of the β1-AR C-terminus; this scaffold targets PKA to phosphorylate β1-AR at Ser312, and the PDZ/scaffold complex is required for efficient receptor recycling. Co-immunoprecipitation, mutagenesis of PDZ motif, receptor recycling assays, PKA phosphorylation assays The Journal of biological chemistry High 17170109
2007 AKAP79/150 interacts directly with the CaV1.2 pore-forming subunit and co-targets PKA and calcineurin, conferring bidirectional regulation of L-type current amplitude; anchored calcineurin dominantly suppresses PKA enhancement. Additionally, AKAP79/150 is required for NFATc4 activation via local Ca²⁺ influx through L-type channels. Co-immunoprecipitation, electrophysiology in HEK293 and hippocampal neurons, NFAT reporter assays Neuron High 17640527
2008 AKAP79/150 forms a signaling complex with TRPV1 through binding to a critical region in the TRPV1 C-terminus, and this complex scaffolds PKA, PKC, and calcineurin to mediate sensitization of TRPV1 by inflammatory mediators (bradykinin, PGE2); disruption of AKAP79/150 binding abrogates heat hyperalgesia. Co-immunoprecipitation, deletion mapping of TRPV1 C-terminal binding region, electrophysiology, in vivo hyperalgesia assay Neuron High 18701070
2008 AKAP79 selectively enhances PKC-mediated phosphorylation of GluR1 at Ser831 by localizing PKC near the receptor via SAP97, shifting the dose-dependence for PKC modulation ~20-fold and making low PKC concentrations as effective as much higher CaMKII concentrations. Biochemical phosphorylation assays, electrophysiology in HEK293 cells, AKAP79-SAP97-GluR1 complex characterization The Journal of biological chemistry High 18305116
2010 AKAP5 organizes a caveolin-3-associated signaling module in cardiomyocytes that clusters adenylyl cyclase 5/6, PKA, calcineurin, and a specific subpopulation of CaV1.2 L-type channels; this complex is essential for β-adrenergic stimulation of calcium transients and PKA phosphorylation of ryanodine receptors and phospholamban. In AKAP5 KO, AC5/6 is displaced from caveolin-3 T-tubule complexes. AKAP5 knockout mice, calcium imaging, electrophysiology, co-immunoprecipitation, phosphorylation assays Circulation research High 20671242
2010 AKAP79 interacts with multiple adenylyl cyclase isoforms (AC5, AC6, AC9) via their N-terminal regions, with a reciprocal binding surface on AKAP79 at residues 77–108; loss of AKAP150 decreases AMPA receptor-associated AC activity in brain. Co-immunoprecipitation, FRET (intensity- and lifetime-based) in living cells, peptide competition, brain extracts from AKAP150 KO mice The Journal of biological chemistry High 20231277
2010 AKAP79 anchors a muscarinic-receptor-activated pool of PKC that phosphorylates the KCNQ2 subunit of M-channels to enhance neuronal excitability; AKAP79 also protects anchored PKC from certain ATP-competitive inhibitors, modifying the cellular pharmacology of PKC. Dual fluorescent imaging/patch-clamp, FRET-based kinase activity reporter (CKAR), electrophysiology, pharmacological inhibitor profiling Molecular cell High 20188672
2010 AKAP79/150 directly associates with Ca²⁺-stimulable adenylyl cyclase 8 (AC8) and limits the sensitivity of AC8 to intracellular Ca²⁺, as shown in HEK293 cells, pancreatic insulin-secreting cells, and hippocampal neurons. Co-immunoprecipitation, live-cell Ca²⁺ and cAMP imaging in multiple cell types The Journal of biological chemistry High 20410303
2010 Ca²⁺/calmodulin disrupts AKAP79/150 interaction with KCNQ2–5 (but not KCNQ1) M-type channels at the plasma membrane, preventing AKAP79-mediated sensitization of these channels to muscarinic inhibition; AKAP79 associates with M1 and AT1 receptors and KCNQ2/3 channels as shown by TIRF/FRET. TIRF/FRET microscopy, perforated patch-clamp electrophysiology, KCNQ subunit mutagenesis (T553A), dominant-negative calmodulin The Journal of neuroscience High 20147557
2010 AKAP5 deletion in hippocampal and striatal neurons causes delocalization of PKA to dendritic shafts with increased binding to MAP2; the PKA-binding domain of AKAP5 is specifically required to maintain PKA near postsynaptic sites for synaptic plasticity and operant learning. AKAP5 KO and D36 (PKA-binding domain deletion) knock-in mice, electrophysiology, behavioral assays, immunofluorescence PloS one High 20428246
2011 AKAP79 dimerizes (stabilized by K328–K328 and K333–K333 cross-links) and, upon addition of Ca²⁺/CaM, assembles a 466-kDa complex comprising dimeric AKAP79 coordinating two RII homodimers, four PP2B heterodimers, and two CaM molecules; Ca²⁺/CaM binding generates a second interface for PP2B, activating anchored phosphatase. Native mass spectrometry, chemical cross-linking, quantitative biochemical reconstitution Proceedings of the National Academy of Sciences of the United States of America High 21464287
2011 Palmitoylation of AKAP79 at two N-terminal cysteines is required for targeting to lipid rafts in HEK293 cells; loss of palmitoylation excludes AKAP79 from rafts, alters membrane diffusion, and abolishes AKAP79-dependent regulation of SOCE-stimulated AC8 activity and PKA-dependent phosphorylation of raft proteins. Mutagenesis of palmitoylation cysteines, pharmacological depalmitoylation, sucrose density fractionation (lipid raft isolation), FRAP, AC activity assays The Journal of biological chemistry High 21771783
2011 AKAP79/150 anchors PKA to regulate Kv4.2 (A-type K⁺ channel) surface expression in hippocampal neurons; the Kv4.2 C-terminal domain interacts with an internal region of AKAP79/150 overlapping its MAGUK-binding domain, and disrupting PKA anchoring decreases neuronal excitability while blocking calcineurin dephosphorylation increases excitability. Co-immunoprecipitation, surface biotinylation assay, patch-clamp electrophysiology, PKA anchoring disruption (Ht31 peptide) The Journal of neuroscience High 21273417
2011 AKAP79 is a novel PP1 regulatory subunit: it directly binds PP1 via a consensus FxxR/KxR/K motif in its first 44 amino acids (enhancing PP1 activity) and a second inhibitory domain at residues 150–250; AKAP79 inhibition of PP1 is substrate-dependent. Co-immunoprecipitation from rat brain, pulldown with purified proteins, PP1 activity assays, surface plasmon resonance, deletion mutagenesis Biochemistry High 21561082
2012 The IAIIIT anchoring motif in human AKAP79 (residues 337–343) binds the same surface of calcineurin as the PxIxIT recognition peptide of NFAT; higher-affinity AKAP–calcineurin interaction impairs NFAT activation by slowing calcineurin release and sequestering it at decoy sites, revealing an optimal affinity window for NFAT signaling. Structural analysis, mutagenesis of anchoring sequence, calcineurin binding assays, NFAT reporter assays in hippocampal neurons Nature structural & molecular biology High 22343722
2012 AKAP79 recruits and scaffolds an AC8–AKAP79–PKA signaling complex; PKA phosphorylates AC8 at Ser112 to provide feedback inhibition of Ca²⁺-stimulated cAMP synthesis, reducing the on-rate of cAMP production during Ca²⁺ oscillations. Site-directed mutagenesis (Ser112), live-cell cAMP imaging during Ca²⁺ oscillations, co-immunoprecipitation Journal of cell science High 22976297
2012 CaMKIIα phosphorylates a specific SAP97 splice variant (containing I3 and I5 inserts) to disrupt its interaction with AKAP79/150, thereby disengaging AKAP79/150 from regulating GluR1 AMPA receptors. Co-immunoprecipitation, in vitro and cell-based phosphorylation assays, GST pulldowns of splice variants, electrophysiology in HEK293 cells The Journal of biological chemistry High 19858198
2012 AKAP79/150 interacts with the neuronal calcium-binding protein caldendrin; caldendrin and calmodulin compete for a partially overlapping binding site on AKAP79 (B-domain), with different Ca²⁺ dependencies—calmodulin binds only with Ca²⁺ via a simple 1-step mechanism, while caldendrin uses an induced-fit mechanism and can bind independent of Ca²⁺. GST pulldown, surface plasmon resonance biosensor analysis, kinetic interaction modeling Journal of neurochemistry High 22693956 22996592
2012 AKAP79 modulates CaV1.2 L-type channel membrane targeting through relief of an autoinhibitory interaction between the channel's distal C-terminus and the II–III linker; the distal C-terminus of CaV1.2 directly interacts with AKAP79. Mutagenesis of polyproline domains, co-immunoprecipitation, channel membrane expression assay Channels Medium 22677788
2012 AKAP79/150-mediated calcineurin–NFAT signaling drives activity-dependent transcriptional upregulation of KCNQ2/3 M-channels in hippocampal neurons; this requires Ca²⁺ influx through L-type channels and is absent in AKAP150⁻/⁻ mice after seizures. AKAP150 KO mice, in vivo seizure induction, KCNQ2/3 mRNA quantification, NFAT reporter assays Neuron High 23259949
2013 The AKAP79–TRPV1 interaction is mediated by a region on AKAP79 between amino acids 326–336; a peptide from this domain inhibits TRPV1 sensitization in vitro, and a cell-penetrant TAT-linked version inhibits inflammatory hyperalgesia in mice without affecting basal pain thresholds. FRET, co-immunoprecipitation, TRPV1 membrane trafficking assay, in vivo hyperalgesia assay The Journal of neuroscience High 23699529
2013 AKAP5 anchoring of adenylyl cyclase (in addition to PKA) is required for β-adrenergic stimulation of GluA1 Ser845 phosphorylation and for LTP induced by 5-Hz θ-rhythm stimulation; AKAP5 KO (lacking both AC and PKA anchoring) produces much greater impairment than D36 (PKA-binding deletion only). AKAP5 KO and D36 knock-in mice, phosphorylation assays, hippocampal slice electrophysiology (LTP), β-adrenergic stimulation The Journal of biological chemistry High 23649627
2014 AKAP5-anchored PKA controls GluA1 S845 phosphorylation and AMPAR surface trafficking during homeostatic scaling; PKA is lost from synapses during scaling down and enriched during scaling up; knockdown of AKAP5 blocks scaling up. siRNA knockdown of AKAP5, FRET-based PKA activity reporters, GluA1 S845 phosphorylation assays, surface AMPAR assays, GluA1 S845 knockin mice Neuron High 25451194
2015 The recycling endosome-resident palmitoyl acyltransferase DHHC2 interacts with and palmitoylates AKAP79/150, targeting it to recycling endosomes in dendrites; DHHC2 knockdown disrupts recycling endosome exocytosis, spine enlargement, AKAP recruitment to spines, and LTP-induced AMPAR synaptic potentiation. RNAi knockdown, palmitoylation assay, dendritic exocytosis assay, spine morphology, AMPAR synaptic current recordings, rescue with lipidated AKAP mutant The Journal of neuroscience High 25589740
2015 AKAP79-anchored PKA phosphorylates STIM1 at T389 in the plasma membrane pool; this phosphorylation is specifically required for activation of store-independent ARC channels (but actually inhibits STIM1-dependent CRAC channel activation), demonstrating selective regulation of two co-existing Orai channel types. Site-directed mutagenesis (T389A), co-immunoprecipitation, patch-clamp electrophysiology, knockdown of AKAP79 The Journal of physiology High 25504574
2017 Intrinsic disorder in AKAP79 produces an ensemble of AKAP79–PP2B configurations; a short linear motif (residues 337–343) is the sole PP2B-anchoring determinant; Ca²⁺/CaM engagement of additional surfaces (including Leu-Lys-Ile-Pro, residues 125–128) condenses configurational variants and fine-tunes phosphatase activity and cyclosporin sensitivity. Negative-stain electron microscopy, chemical cross-linking, live-cell fluorescent activity sensors (NFAT translocation), site-directed mutagenesis eLife High 28967377
2017 LTD-induced synaptic removal of AKAP79/150 requires CaMKII activity and depalmitoylation of two N-terminal Cys residues; CaMKII phosphorylates AKAP79/150's N-terminal polybasic domain (inhibiting F-actin association) preferentially via autonomous (Thr286-autophosphorylated) CaMKII; Ca²⁺/CaM binding to the substrate sites protects them from phosphorylation in the presence of strong LTP stimuli, providing stimulus-selective regulation. CaMKII inhibitors and knockout, LTD induction in hippocampal neurons, palmitoylation assay, spine morphology, actin-binding assay, phospho-site mutagenesis The Journal of biological chemistry High 29196604
2019 AKAP79 recruits the transcription factor NFAT via a C-terminal leucine-zipper (LZ) domain, forming a direct AKAP79–NFAT complex at the plasma membrane; this LZ-mediated NFAT recruitment (not the LTCC–AKAP interaction per se) is required for depolarization-induced NFAT signaling in hippocampal neurons. RNAi knockdown + replacement with LZ-deletion mutant, co-immunoprecipitation, FRET, Ca²⁺ imaging, FRAP, fluorescence correlation spectroscopy, electrophysiology Molecular biology of the cell High 31091162
2020 AKAP5 organizes a nanocomplex containing P2Y11/P2Y11-like receptors, AC5, PKA, and CaV1.2 at the plasma membrane of arterial myocytes; disruption of AKAP5 blocks glucose- and P2Y11-induced cAMP synthesis, CaV1.2 potentiation, and vasoconstriction. AKAP5 KO mice, calcium imaging, proximity ligation assay, TIRF microscopy, patch-clamp, myography Nature communications High 33082339
2020 STIM2 recruits Orai1/STIM1 to ER–PM junctions and promotes assembly with AKAP79 to couple Orai1 channel function to NFAT1 activation; STIM2 polybasic domain mediates this assembly. Loss of STIM2 impairs NFAT1 activation and Orai1–AKAP79 association without significantly affecting global Ca²⁺. Co-immunoprecipitation, knockdown, STIM1ΔK mutant, NFAT1 translocation assay, Ca²⁺ imaging Proceedings of the National Academy of Sciences of the United States of America High 32601188
2021 The N-terminus of Orai1 (lacking in Orai2, Orai3, and short Orai1) contains an AKAP79-interaction site required for excitation-transcription coupling; NMR reveals a compact, proline-driven structure at this site; disrupting Orai1–AKAP79 interaction suppresses cytokine production without affecting other Orai1 functions. NMR structural analysis, co-immunoprecipitation, NFAT1 translocation assay, cytokine production assay, Orai isoform comparison Proceedings of the National Academy of Sciences of the United States of America High 33941685
2021 AKAP79 increases the rate of calcineurin dephosphorylation of type II PKA regulatory (RII) subunits by ~10-fold, enabling calcineurin to suppress PKA activity without altering cAMP levels by increasing catalytic subunit capture rate; kinetic modeling and hippocampal neuron experiments indicate this contributes to LTD. In vitro phosphatase activity assay, fluorescent PKA activity reporter, kinetic modeling, hippocampal neuron electrophysiology eLife High 34612814
2021 AKAP79/150 coordinates leptin-induced PKA signaling at the cell membrane to regulate KATP channel trafficking in pancreatic β-cells; AKAP79/150 knockdown abolishes leptin-induced membrane PKA activity increases; disrupting PP2B anchoring to AKAP79/150 elevates basal PKA signaling and increases surface KATP channels. FRET-based PKA reporters, siRNA knockdown, KATP channel surface assay, co-immunoprecipitation The Journal of biological chemistry High 33617875
2010 AKAP79/150 pre-assembled with RXFP1 (relaxin receptor), AC2, β-arrestin 2, and PDE4D3 forms a constitutively active signalosome; AC2 is functionally coupled to RXFP1 through AKAP79 binding to helix 8 of RXFP1; PKA-activated PDE4D3 (via β-arrestin 2 on Ser704 of RXFP1) provides tonic opposition to cAMP, enabling sub-picomolar relaxin signaling. Co-immunoprecipitation, cAMP biosensors in single cells, deletion mapping, mutagenesis The EMBO journal High 20664520
2019 AKAP79-anchored PKC phosphorylates GluA1 at Ser831, which is sufficient to drive appearance of Ca²⁺-permeable (GluA2-lacking) AMPARs; other AKAP79 signaling components (PKA/calcineurin) and C-terminal phosphorylation sites play a permissive/limiting role. Electrophysiology (I-V relationships), mutagenesis of GluA1 phosphorylation sites, AKAP79 deletion mutants in HEK293 cells The Journal of biological chemistry High 30737285

Source papers

Stage 0 corpus · 91 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1996 Coordination of three signaling enzymes by AKAP79, a mammalian scaffold protein. Science (New York, N.Y.) 479 8599116
2007 AKAP79/150 anchoring of calcineurin controls neuronal L-type Ca2+ channel activity and nuclear signaling. Neuron 284 17640527
2008 Proinflammatory mediators modulate the heat-activated ion channel TRPV1 via the scaffolding protein AKAP79/150. Neuron 217 18701070
1998 Membrane-targeting sequences on AKAP79 bind phosphatidylinositol-4, 5-bisphosphate. The EMBO journal 204 9545238
2002 Regulation of GluR1 by the A-kinase anchoring protein 79 (AKAP79) signaling complex shares properties with long-term depression. The Journal of neuroscience : the official journal of the Society for Neuroscience 183 11943807
2005 RNA silencing identifies PDE4D5 as the functionally relevant cAMP phosphodiesterase interacting with beta arrestin to control the protein kinase A/AKAP79-mediated switching of the beta2-adrenergic receptor to activation of ERK in HEK293B2 cells. The Journal of biological chemistry 169 16030021
2010 Sympathetic stimulation of adult cardiomyocytes requires association of AKAP5 with a subpopulation of L-type calcium channels. Circulation research 140 20671242
2001 Regulation of membrane targeting of the G protein-coupled receptor kinase 2 by protein kinase A and its anchoring protein AKAP79. The Journal of biological chemistry 134 11278469
2014 PKA-GluA1 coupling via AKAP5 controls AMPA receptor phosphorylation and cell-surface targeting during bidirectional homeostatic plasticity. Neuron 132 25451194
2012 Balanced interactions of calcineurin with AKAP79 regulate Ca2+-calcineurin-NFAT signaling. Nature structural & molecular biology 129 22343722
2002 Mapping the protein phosphatase-2B anchoring site on AKAP79. Binding and inhibition of phosphatase activity are mediated by residues 315-360. The Journal of biological chemistry 124 12354762
2002 Trafficking of L-type calcium channels mediated by the postsynaptic scaffolding protein AKAP79. The Journal of biological chemistry 112 12114507
2000 AKAP79 and the evolution of the AKAP model. FEBS letters 112 10878251
2002 Imaging kinase--AKAP79--phosphatase scaffold complexes at the plasma membrane in living cells using FRET microscopy. The Journal of cell biology 109 12507994
1997 Regulation of the AKAP79-protein kinase C interaction by Ca2+/Calmodulin. The Journal of biological chemistry 99 9202019
2010 Interaction with AKAP79 modifies the cellular pharmacology of PKC. Molecular cell 96 20188672
2010 AKAP79 interacts with multiple adenylyl cyclase (AC) isoforms and scaffolds AC5 and -6 to alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA) receptors. The Journal of biological chemistry 95 20231277
1993 Characterization of distinct tethering and intracellular targeting domains in AKAP75, a protein that links cAMP-dependent protein kinase II beta to the cytoskeleton. The Journal of biological chemistry 79 8509414
2011 Architecture and dynamics of an A-kinase anchoring protein 79 (AKAP79) signaling complex. Proceedings of the National Academy of Sciences of the United States of America 78 21464287
1999 Mechanism of A-kinase-anchoring protein 79 (AKAP79) and protein kinase C interaction. The Biochemical journal 75 10510312
2011 Palmitoylation targets AKAP79 protein to lipid rafts and promotes its regulation of calcium-sensitive adenylyl cyclase type 8. The Journal of biological chemistry 74 21771783
2010 Mutations in AKAP5 disrupt dendritic signaling complexes and lead to electrophysiological and behavioral phenotypes in mice. PloS one 73 20428246
2012 Activity-dependent transcriptional regulation of M-Type (Kv7) K(+) channels by AKAP79/150-mediated NFAT actions. Neuron 72 23259949
1998 AKAP79 inhibits calcineurin through a site distinct from the immunophilin-binding region. The Journal of biological chemistry 72 9765270
2006 AKAP79-mediated targeting of the cyclic AMP-dependent protein kinase to the beta1-adrenergic receptor promotes recycling and functional resensitization of the receptor. The Journal of biological chemistry 71 16940053
2010 Sub-picomolar relaxin signalling by a pre-assembled RXFP1, AKAP79, AC2, beta-arrestin 2, PDE4D3 complex. The EMBO journal 67 20664520
2010 AKAP79/150 interacts with AC8 and regulates Ca2+-dependent cAMP synthesis in pancreatic and neuronal systems. The Journal of biological chemistry 66 20410303
2006 Assembly of an SAP97-AKAP79-cAMP-dependent protein kinase scaffold at the type 1 PSD-95/DLG/ZO1 motif of the human beta(1)-adrenergic receptor generates a receptosome involved in receptor recycling and networking. The Journal of biological chemistry 65 17170109
2015 The palmitoyl acyltransferase DHHC2 regulates recycling endosome exocytosis and synaptic potentiation through palmitoylation of AKAP79/150. The Journal of neuroscience : the official journal of the Society for Neuroscience 61 25589740
2013 Adenylyl cyclase anchoring by a kinase anchor protein AKAP5 (AKAP79/150) is important for postsynaptic β-adrenergic signaling. The Journal of biological chemistry 58 23649627
2001 Targeting of an A kinase-anchoring protein, AKAP79, to an inwardly rectifying potassium channel, Kir2.1. The Journal of biological chemistry 56 11287423
2014 G protein-coupled receptor 30 (GPR30) forms a plasma membrane complex with membrane-associated guanylate kinases (MAGUKs) and protein kinase A-anchoring protein 5 (AKAP5) that constitutively inhibits cAMP production. The Journal of biological chemistry 53 24962572
2010 Ca2+/calmodulin disrupts AKAP79/150 interactions with KCNQ (M-Type) K+ channels. The Journal of neuroscience : the official journal of the Society for Neuroscience 53 20147557
2011 AKAP79/150 signal complexes in G-protein modulation of neuronal ion channels. The Journal of neuroscience : the official journal of the Society for Neuroscience 50 21562284
2021 The N terminus of Orai1 couples to the AKAP79 signaling complex to drive NFAT1 activation by local Ca2+ entry. Proceedings of the National Academy of Sciences of the United States of America 47 33941685
2011 AKAP79/150 impacts intrinsic excitability of hippocampal neurons through phospho-regulation of A-type K+ channel trafficking. The Journal of neuroscience : the official journal of the Society for Neuroscience 46 21273417
2008 AKAP79 selectively enhances protein kinase C regulation of GluR1 at a Ca2+-calmodulin-dependent protein kinase II/protein kinase C site. The Journal of biological chemistry 46 18305116
2008 Stable membrane expression of postsynaptic CaV1.2 calcium channel clusters is independent of interactions with AKAP79/150 and PDZ proteins. The Journal of neuroscience : the official journal of the Society for Neuroscience 46 19091974
2004 Modulation of dopamine mediated phosphorylation of AMPA receptors by PSD-95 and AKAP79/150. Neuropharmacology 46 15458848
2017 CaMKII regulates the depalmitoylation and synaptic removal of the scaffold protein AKAP79/150 to mediate structural long-term depression. The Journal of biological chemistry 45 29196604
2009 Ca2+/calmodulin-dependent protein kinase II binds to and phosphorylates a specific SAP97 splice variant to disrupt association with AKAP79/150 and modulate alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-type glutamate receptor (AMPAR) activity. The Journal of biological chemistry 45 19858198
2013 Role of AKAP79/150 protein in β1-adrenergic receptor trafficking and signaling in mammalian cells. The Journal of biological chemistry 44 24121510
2013 Mapping the binding site of TRPV1 on AKAP79: implications for inflammatory hyperalgesia. The Journal of neuroscience : the official journal of the Society for Neuroscience 40 23699529
2020 AKAP5 complex facilitates purinergic modulation of vascular L-type Ca2+ channel CaV1.2. Nature communications 37 33082339
2006 G-Protein-coupled receptor-associated A-kinase anchoring proteins: AKAP79 and AKAP250 (gravin). European journal of cell biology 37 16442664
2020 STIM2 targets Orai1/STIM1 to the AKAP79 signaling complex and confers coupling of Ca2+ entry with NFAT1 activation. Proceedings of the National Academy of Sciences of the United States of America 36 32601188
2005 Beta-arrestin-recruited phosphodiesterase-4 desensitizes the AKAP79/PKA-mediated switching of beta2-adrenoceptor signalling to activation of ERK. Biochemical Society transactions 35 16246112
2008 G-protein-coupled receptor-associated A-kinase anchoring proteins AKAP5 and AKAP12: differential signaling to MAPK and GPCR recycling. Journal of molecular signaling 33 19055733
2003 Identification of an IQGAP1/AKAP79 complex in beta-cells. Journal of cellular biochemistry 32 12938160
2000 Localization of the A kinase anchoring protein AKAP79 in the human hippocampus. The European journal of neuroscience 31 10762347
2019 AKAP79/150 recruits the transcription factor NFAT to regulate signaling to the nucleus by neuronal L-type Ca2+ channels. Molecular biology of the cell 30 31091162
2014 Carvedilol reverses cardiac insufficiency in AKAP5 knockout mice by normalizing the activities of calcineurin and CaMKII. Cardiovascular research 30 25225170
2012 A key phosphorylation site in AC8 mediates regulation of Ca(2+)-dependent cAMP dynamics by an AC8-AKAP79-PKA signalling complex. Journal of cell science 29 22976297
2013 AKAP79, PKC, PKA and PDE4 participate in a Gq-linked muscarinic receptor and adenylate cyclase 2 cAMP signalling complex. The Biochemical journal 27 23889134
2017 Intrinsic disorder within AKAP79 fine-tunes anchored phosphatase activity toward substrates and drug sensitivity. eLife 24 28967377
2015 Anchoring protein AKAP79-mediated PKA phosphorylation of STIM1 determines selective activation of the ARC channel, a store-independent Orai channel. The Journal of physiology 24 25504574
2010 Ca2+/calmodulin-dependent protein kinase II inhibitors disrupt AKAP79-dependent PKC signaling to GluA1 AMPA receptors. The Journal of biological chemistry 24 21156788
2011 A Potential Role for a Genetic Variation of AKAP5 in Human Aggression and Anger Control. Frontiers in human neuroscience 22 22232585
2008 G-protein-coupled receptor-associated A-kinase anchoring proteins AKAP5 and AKAP12: differential trafficking and distribution. Cellular signalling 19 18950703
2011 Identification of AKAP79 as a protein phosphatase 1 catalytic binding protein. Biochemistry 18 21561082
2005 Differential expression of protein kinase A, AKAP79, and PP2B in pregnant human myometrial membranes prior to and during labor. Journal of the Society for Gynecologic Investigation 18 15914039
2021 AKAP79 enables calcineurin to directly suppress protein kinase A activity. eLife 16 34612814
2021 AKAP79 Orchestrates a Cyclic AMP Signalosome Adjacent to Orai1 Ca2+ Channels. Function (Oxford, England) 15 34458850
2015 Curcumin Protects Neurons from Glutamate-Induced Excitotoxicity by Membrane Anchored AKAP79-PKA Interaction Network. Evidence-based complementary and alternative medicine : eCAM 15 26170881
2019 Preferential generation of Ca2+-permeable AMPA receptors by AKAP79-anchored protein kinase C proceeds via GluA1 subunit phosphorylation at Ser-831. The Journal of biological chemistry 14 30737285
2012 AKAP79 modulation of L-type channels involves disruption of intramolecular interactions in the CaV1.2 subunit. Channels (Austin, Tex.) 14 22677788
2012 AKAP79/150 interacts with the neuronal calcium-binding protein caldendrin. Journal of neurochemistry 14 22693956
2011 AKAP12 and AKAP5 form higher-order hetero-oligomers. Journal of molecular signaling 14 21831305
2021 AKAP79/150 coordinates leptin-induced PKA signaling to regulate KATP channel trafficking in pancreatic β-cells. The Journal of biological chemistry 13 33617875
2015 Mechanisms and dynamics of AKAP79/150-orchestrated multi-protein signalling complexes in brain and peripheral nerve. The Journal of physiology 13 25653013
2018 Targeting FRET-Based Reporters for cAMP and PKA Activity Using AKAP79. Sensors (Basel, Switzerland) 12 29976855
2011 AKAP5 and AKAP12 Form Homo-oligomers. Journal of molecular signaling 12 21554706
2013 Increased density of AKAP5-expressing neurons in the anterior cingulate cortex of subjects with bipolar disorder. Journal of psychiatric research 11 23462372
2010 The contribution of AKAP5 in amylase secretion from mouse parotid acini. American journal of physiology. Cell physiology 9 20164376
2022 Nuanced Interactions between AKAP79 and STIM1 with Orai1 Ca2+ Channels at Endoplasmic Reticulum-Plasma Membrane Junctions Sustain NFAT Activation. Molecular and cellular biology 8 36317924
2012 Kinetic and mechanistic differences in the interactions between caldendrin and calmodulin with AKAP79 suggest different roles in synaptic function. Journal of molecular recognition : JMR 8 22996592
2003 Expression and intracellular localization of protein phosphatases 2A and 2B, protein kinase a, A-Kinase anchoring protein (AKAP79), and binding of the regulatory (RII) subunit of protein kinase a to AKAP79 in human myometrium. Journal of the Society for Gynecologic Investigation 7 14519485
2015 Modified sympathetic nerve regulation in AKAP5-null mice. Biochemical and biophysical research communications 5 26713362
2014 AKAP5 keeps L-type channels and NFAT on their toes. Cell reports 5 24926793
2001 Development-related expression of AKAP79 in the striatal compartments of the human brain. Cells, tissues, organs 5 11275698
2015 AKAP5 signaling complexes: focal points and functional properties. Neuro endocrinology letters 4 25789584
2012 "Shaping" of cell signaling via AKAP-tethered PDE4D: Probing with AKAR2-AKAP5 biosensor. Journal of molecular signaling 4 22583680
2006 Contextual utilization of enzymes in discrete AKAP79/150 signalling complexes. European journal of cell biology 4 16460836
2024 Akap5 links synaptic dysfunction to neuroinflammatory signaling in a mouse model of infantile neuronal ceroid lipofuscinosis. Frontiers in synaptic neuroscience 3 38798824
2020 AKAP5 anchors PKA to enhance regulation of the HERG channel. The international journal of biochemistry & cell biology 3 32173522
2019 Maturation of thalamocortical synapses in the somatosensory cortex depends on neocortical AKAP5 expression. Neuroscience letters 3 31310785
2004 AKAP79 increases the functional expression of skeletal muscle Ca2+ channels in Xenopus oocytes. Biochemical and biophysical research communications 3 15003529
2022 Metoprolol Mitigates Ischemic Heart Remodeling and Fibrosis by Increasing the Expression of AKAP5 in Ischemic Heart. Oxidative medicine and cellular longevity 2 36238650
2025 Unveiling the significance of AKAP79/150 in the nervous system disorders: An emerging opportunity for future therapies? Neurobiology of disease 1 39864527
2026 Maternal exercise improves vascular function in hypertensive offspring via A-kinase anchoring protein 150 gene (Akap5) epigenetic modifications. British journal of pharmacology 0 41640285
2023 Retracted: Metoprolol Mitigates Ischemic Heart Remodeling and Fibrosis by Increasing the Expression of AKAP5 in Ischemic Heart. Oxidative medicine and cellular longevity 0 37810553