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    Akap5 A kinase anchor protein 5 [ Mus musculus (house mouse) ]

    Gene ID: 238276, updated on 18-Sep-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Regulation of depressive-like behaviours by palmitoylation: Role of AKAP150 in the basolateral amygdala.

    Regulation of depressive-like behaviours by palmitoylation: Role of AKAP150 in the basolateral amygdala.
    Wang SY, Xia ZX, Yang SW, Chen WK, Zhao YL, Li MD, Tian D, Pan Y, Lin XS, Zhu XQ, Huang Z, Liu JM, Lai ZM, Tao WC, Shen ZC.

    06/12/2024
    AKAP150-anchored PKA regulates synaptic transmission and plasticity, neuronal excitability and CRF neuromodulation in the mouse lateral habenula.

    AKAP150-anchored PKA regulates synaptic transmission and plasticity, neuronal excitability and CRF neuromodulation in the mouse lateral habenula.
    Simmons SC, Flerlage WJ, Langlois LD, Shepard RD, Bouslog C, Thomas EH, Gouty KM, Sanderson JL, Gouty S, Cox BM, Dell'Acqua ML, Nugent FS., Free PMC Article

    03/25/2024
    Selective activation of AKAP150/TRPV1 in ventrolateral periaqueductal gray GABAergic neurons facilitates conditioned place aversion in male mice.

    Selective activation of AKAP150/TRPV1 in ventrolateral periaqueductal gray GABAergic neurons facilitates conditioned place aversion in male mice.
    Bai X, Zhang K, Ou C, Nie B, Zhang J, Huang Y, Zhang Y, Huang J, Ouyang H, Cao M, Huang W., Free PMC Article

    07/24/2023
    Proteasomal-Mediated Degradation of AKAP150 Accompanies AMPAR Endocytosis during cLTD.

    Proteasomal-Mediated Degradation of AKAP150 Accompanies AMPAR Endocytosis during cLTD.
    Cheng W, Siedlecki-Wullich D, Català-Solsona J, Fábregas C, Fadó R, Casals N, Solé M, Unzeta M, Saura CA, Rodríguez-Alvarez J, Miñano-Molina AJ., Free PMC Article

    07/31/2021
    Sensitization of glutamate receptor-mediated pain behaviour via nerve growth factor-dependent phosphorylation of transient receptor potential V1 under inflammatory conditions.

    Sensitization of glutamate receptor-mediated pain behaviour via nerve growth factor-dependent phosphorylation of transient receptor potential V1 under inflammatory conditions.
    Masuoka T, Yamashita Y, Yoshida J, Nakano K, Tawa M, Nishio M, Ishibashi T., Free PMC Article

    05/29/2021
    Knockout of AKAP150 improves impaired BK channel-mediated vascular dysfunction through the Akt/GSK3beta signalling pathway in diabetes mellitus.

    Knockout of AKAP150 improves impaired BK channel-mediated vascular dysfunction through the Akt/GSK3β signalling pathway in diabetes mellitus.
    Zhu YR, Jiang XX, Ye P, Wang ZM, Zheng Y, Liu Z, Chen SL, Zhang DM., Free PMC Article

    05/1/2021
    AKAP5 complex facilitates purinergic modulation of vascular L-type Ca(2+) channel CaV1.2.

    AKAP5 complex facilitates purinergic modulation of vascular L-type Ca(2+) channel Ca(V)1.2.
    Prada MP, Syed AU, Reddy GR, Martín-Aragón Baudel M, Flores-Tamez VA, Sasse KC, Ward SM, Sirish P, Chiamvimonvat N, Bartels P, Dickson EJ, Hell JW, Scott JD, Santana LF, Xiang YK, Navedo MF, Nieves-Cintrón M., Free PMC Article

    11/28/2020
    Maturation of thalamocortical synapses in the somatosensory cortex depends on neocortical AKAP5 expression.

    Maturation of thalamocortical synapses in the somatosensory cortex depends on neocortical AKAP5 expression.
    Zhang M, Lu M, Huang H, Liu X, Su H, Li H.

    09/26/2020
    AKAP150-PKA directly modulates basolateral amygdala neuronal synaptic strength

    A-Kinase Anchoring Protein 150 and Protein Kinase A Complex in the Basolateral Amygdala Contributes to Depressive-like Behaviors Induced by Chronic Restraint Stress.
    Zhou HY, He JG, Hu ZL, Xue SG, Xu JF, Cui QQ, Gao SQ, Zhou B, Wu PF, Long LH, Wang F, Chen JG.

    06/13/2020
    AKAP150 palmitoylation controls its subcellular localization to maintain proper basal and activity-dependent regulation of synaptic AMPAR subunit composition.

    AKAP150 Palmitoylation Regulates Synaptic Incorporation of Ca(2+)-Permeable AMPA Receptors to Control LTP.
    Purkey AM, Woolfrey KM, Crosby KC, Stich DG, Chick WS, Aoto J, Dell'Acqua ML., Free PMC Article

    11/16/2019
    AKAP150 regulates Ca(2+ )cycling and myocardial ionotropy following pathological stress, promoting pathological remodelling and heart failure propensity.

    Loss of AKAP150 promotes pathological remodelling and heart failure propensity by disrupting calcium cycling and contractile reserve.
    Li L, Li J, Drum BM, Chen Y, Yin H, Guo X, Luckey SW, Gilbert ML, McKnight GS, Scott JD, Santana LF, Liu Q., Free PMC Article

    10/14/2017
    AKAP150-calcineurin signaling dyad is essential for the activation of the phosphatase and the subsequent down-regulation of Kv channel currents following myocardial infarction.

    AKAP150 participates in calcineurin/NFAT activation during the down-regulation of voltage-gated K(+) currents in ventricular myocytes following myocardial infarction.
    Nieves-Cintrón M, Hirenallur-Shanthappa D, Nygren PJ, Hinke SA, Dell'Acqua ML, Langeberg LK, Navedo M, Santana LF, Scott JD., Free PMC Article

    02/25/2017
    This study demonstrated that the AKAP150 oordinates metabotropic glutamate receptor sensitization of peripheral sensory neurons.

    A-kinase anchoring protein 79/150 coordinates metabotropic glutamate receptor sensitization of peripheral sensory neurons.
    Szteyn K, Rowan MP, Gomez R, Du J, Carlton SM, Jeske NA., Free PMC Article

    07/30/2016
    Thus, our present study revealed that AKAP5 plays a significant role in the regulation of sympathetic nerve activities.

    Modified sympathetic nerve regulation in AKAP5-null mice.
    Han C, Tomita H, Ohba T, Nishizaki K, Ogata Y, Matsuzaki Y, Sawamura D, Yanagisawa T, Osanai T, Imaizumi T, Matsubara A, Adachi T, Ono K, Okumura K, Murakami M.

    05/28/2016
    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.

    Carvedilol reverses cardiac insufficiency in AKAP5 knockout mice by normalizing the activities of calcineurin and CaMKII.
    Li X, Matta SM, Sullivan RD, Bahouth SW., Free PMC Article

    11/28/2015
    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

    AKAP150-dependent cooperative TRPV4 channel gating is central to endothelium-dependent vasodilation and is disrupted in hypertension.
    Sonkusare SK, Dalsgaard T, Bonev AD, Hill-Eubanks DC, Kotlikoff MI, Scott JD, Santana LF, Nelson MT., Free PMC Article

    04/4/2015
    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.

    AKAP150 contributes to enhanced vascular tone by facilitating large-conductance Ca2+-activated K+ channel remodeling in hyperglycemia and diabetes mellitus.
    Nystoriak MA, Nieves-Cintrón M, Nygren PJ, Hinke SA, Nichols CB, Chen CY, Puglisi JL, Izu LT, Bers DM, Dell'acqua ML, Scott JD, Santana LF, Navedo MF., Free PMC Article

    04/26/2014
    a significant role for the AKAP5 scaffold in signaling and trafficking of the beta1-AR in cardiac myocytes and mammalian cells.

    Role of AKAP79/150 protein in β1-adrenergic receptor trafficking and signaling in mammalian cells.
    Li X, Nooh MM, Bahouth SW., Free PMC Article

    02/8/2014
    Anchoring of protein kinase A and adenylyl cyclase by AKAP5 is important for regulation of postsynaptic functions and specifically AMPA receptor activity.

    Adenylyl cyclase anchoring by a kinase anchor protein AKAP5 (AKAP79/150) is important for postsynaptic β-adrenergic signaling.
    Zhang M, Patriarchi T, Stein IS, Qian H, Matt L, Nguyen M, Xiang YK, Hell JW., Free PMC Article

    08/31/2013
    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.

    Scaffolding by A-kinase anchoring protein enhances functional coupling between adenylyl cyclase and TRPV1 channel.
    Efendiev R, Bavencoffe A, Hu H, Zhu MX, Dessauer CW., Free PMC Article

    04/20/2013
    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.

    Activity-dependent transcriptional regulation of M-Type (Kv7) K(+) channels by AKAP79/150-mediated NFAT actions.
    Zhang J, Shapiro MS., Free PMC Article

    03/2/2013
    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.

    Anchored phosphatases modulate glucose homeostasis.
    Hinke SA, Navedo MF, Ulman A, Whiting JL, Nygren PJ, Tian G, Jimenez-Caliani AJ, Langeberg LK, Cirulli V, Tengholm A, Dell'Acqua ML, Santana LF, Scott JD., Free PMC Article

    01/26/2013
    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.

    AKAP150-anchored calcineurin regulates synaptic plasticity by limiting synaptic incorporation of Ca2+-permeable AMPA receptors.
    Sanderson JL, Gorski JA, Gibson ES, Lam P, Freund RK, Chick WS, Dell'Acqua ML., Free PMC Article

    01/12/2013
    A kinase anchor protein 150 (AKAP150)-associated protein kinase A limits dendritic spine density

    A kinase anchor protein 150 (AKAP150)-associated protein kinase A limits dendritic spine density.
    Lu Y, Zha XM, Kim EY, Schachtele S, Dailey ME, Hall DD, Strack S, Green SH, Hoffman DA, Hell JW., Free PMC Article

    10/1/2011
    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.

    Restoration of normal L-type Ca2+ channel function during Timothy syndrome by ablation of an anchoring protein.
    Cheng EP, Yuan C, Navedo MF, Dixon RE, Nieves-Cintrón M, Scott JD, Santana LF., Free PMC Article

    09/24/2011
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