Psychiatry related information on Akap5

• Interestingly, strong generalized stimulation produced by electroconvulsive shock did not increase the expression of AKAP-150 [1].

High impact information on Akap5

• Here we show that the regulatory subunits of PKA are colocalized with AKAP150 (an AKAP isoform that is expressed in the brain) in the lateral amygdala (LA) and that infusion to the LA of the peptide St-Ht31, which blocks PKA anchoring onto AKAPs, impairs memory consolidation of auditory fear conditioning [2].
• The protocol involves a sequence of: (a) ammonium sulfate precipitation, (b) DEAE-cellulose ion exchange chromatography, (c) gel filtration chromatography on Bio-Gel P150 in 1.0 M ammonium acetate, (d) hydrophobic chromatography on dodecyl agarose, and (e) gel filtration chromatography in 6.0 M guanidine hydrochloride [3].
• AKAP 150 is abundant in Purkinje cells and in neurons of the olfactory bulb, basal ganglia, cerebral cortex, and other forebrain regions [4].
• cAMP signaling in neurons: patterns of neuronal expression and intracellular localization for a novel protein, AKAP 150, that anchors the regulatory subunit of cAMP-dependent protein kinase II beta [4].
• A high proportion of total AKAP 150 is concentrated in primary branches of dendrites, where it is associated with microtubules [4].

Biological context of Akap5

• High affinity binding protein for the regulatory subunit of cAMP-dependent protein kinase II-B. Cloning, characterization, and expression of cDNAs for rat brain P150 [5].
• LTP but not seizure is associated with up-regulation of AKAP-150 [1].
• Expression of AKAP-150 and quick down-regulation of Na(+),K(+)-ATPase by AKAP-anchored PKA in response to cAMP elevation are characteristics specific to PG among the three major salivary glands, suggesting the presence of PG-specific regulatory mechanisms for saliva production/secretion [6].
• Thus, the mechanisms behind exercise training-enhanced adipocyte lipolysis could involve the increased activities of PKA and HSL with enhanced expressions of AKAP150 and some subunits of PKA, all of which may be compartmentalized within adipocytes [7].

Anatomical context of Akap5

• Regulation of Na,K-ATPase by cAMP-dependent protein kinase anchored on membrane via A-kinase anchoring protein subtype, AKAP-150, in rat parotid gland [8].
• The results suggest that bifunctional AKAP 150 tethers PKAII beta to the dendritic cytoskeleton, thereby creating a discrete target site for the reception and propagation of signals carried by cAMP [4].
• In contrast, little AKAP 150 is detected in neurons of the thalamus, hypothalamus, midbrain, and hindbrain [4].
• These data indicate that progesterone prevents the decline in PKA associated with myometrial plasma membrane and with AKAP150 in the pregnant rat [9].
• AKAP-150 mRNA has a biphasic modulation in the dentate gyrus following the induction of LTP [1].

Associations of Akap5 with chemical compounds

• In addition, polyproteins encoded by both of these FeSV isolates bound to, and phosphorylated tyrosine acceptor sites within, a 150,000-molecular-weight cellular substrate (P150) [10].
• Moreover, total cellular levels of phosphotyrosine remained unaltered in McDonough FeSV-transformed cells, and the major McDonough FeSV polyprotein translational product lacked binding affinity for P150 [10].
• There was some overlap between AKAP150 and GABA receptor type A receptor beta2/3-immunoreactivity intracellularly in perinuclear clusters [11].
• This implies that the AKAP-150 harbours a novel property of selective responsiveness to the stimulation patterns that trigger NMDA-dependent LTP in vivo [1].
• Its selective up-regulation during LTP and its identified functions as a scaffold for protein kinase A, protein kinase C, calmodulin, calcineurin and ionotropic glutamate receptors suggest that AKAP-150 encodes is an important effector protein in the expression of late LTP [1].

Regulatory relationships of Akap5

• The NMDA receptor antagonist CPP blocked the tetanus-induced modulation of AKAP-150 expression [1].

Analytical, diagnostic and therapeutic context of Akap5

• Sequence analyses disclosed that P150 is a previously uncharacterized protein that contains multiple octapeptide repeats as well as unique sequences [5].
• AKAP79 also associates with conventional, novel and atypical isoforms of PKC in vitro and in vivo, and immunofluorescence staining of rat hippocampal neurons demonstrates that the murine anchoring-protein homologue AKAP150 is co-distributed with PKCalpha/beta, PKCepsilon or PKCiota [12].
• AKAP-150 protein in BLMVs was shown by immunoblotting and an RII overlay assay and was coimmunoprecipitated by anti-RII antibody [13].
• We have combined this with in situ hybridization and have identified A-kinase anchoring protein of 150 kDa (AKAP-150) as a gene selectively up-regulated during the maintenance phase of LTP [1].
• The localization of neurofilament triplet proteins in PC12 cells grown in the absence of (PC12-) or maintained in the presence of (PC12+) nerve growth factor (NGF) was studied using indirect immunofluorescence and monospecific, immunosorbent purified antibodies to 68,000 (P68), 150,000 (P150) and 200,000 (P200) dalton neurofilament proteins [14].

References