Mark L Dell Acqua


Affiliation: University of Colorado Denver
Country: USA


  1. Wild A, Sinnen B, Dittmer P, Kennedy M, Sather W, Dell Acqua M. Synapse-to-Nucleus Communication through NFAT Is Mediated by L-type Ca2+ Channel Ca2+ Spike Propagation to the Soma. Cell Rep. 2019;26:3537-3550.e4 pubmed publisher
    ..Together, these data support a model for synapse to nucleus communication where NFAT integrates somatic LTCC Ca2+ spikes to alter transcription during periods of heightened neuronal activity. ..
  2. Gibson E, Woolfrey K, Li H, Hogan P, Nemenoff R, Heasley L, et al. Subcellular Localization and Activity of the Mitogen-Activated Protein Kinase Kinase 7 (MKK7) γ Isoform are Regulated through Binding to the Phosphatase Calcineurin. Mol Pharmacol. 2019;95:20-32 pubmed publisher
  3. Purkey A, Woolfrey K, Crosby K, Stich D, Chick W, Aoto J, et al. AKAP150 Palmitoylation Regulates Synaptic Incorporation of Ca2+-Permeable AMPA Receptors to Control LTP. Cell Rep. 2018;25:974-987.e4 pubmed publisher
    ..Thus, AKAP150 palmitoylation controls its subcellular localization to maintain proper basal and activity-dependent regulation of synaptic AMPAR subunit composition. ..
  4. Woolfrey K, Dell Acqua M. Coordination of Protein Phosphorylation and Dephosphorylation in Synaptic Plasticity. J Biol Chem. 2015;290:28604-12 pubmed publisher
    ..This review will focus on coordination of postsynaptic serine/threonine kinase and phosphatase signaling by scaffold proteins during synaptic plasticity. ..
  5. Woolfrey K, O Leary H, Goodell D, Robertson H, Horne E, Coultrap S, et al. CaMKII regulates the depalmitoylation and synaptic removal of the scaffold protein AKAP79/150 to mediate structural long-term depression. J Biol Chem. 2018;293:1551-1567 pubmed publisher
    ..Additionally, our results provide the first direct evidence for a function of the well-described AKAP79/150 trafficking in regulating LTD-induced spine shrinkage. ..
  6. Wild A, Dell Acqua M. Potential for therapeutic targeting of AKAP signaling complexes in nervous system disorders. Pharmacol Ther. 2018;185:99-121 pubmed publisher
    ..In this review we will discuss the role of AKAPs in both regulating normal nervous system function and dysfunction associated with disease, and the potential for therapeutic targeting of AKAP signaling complexes. ..
  7. Coultrap S, Freund R, O Leary H, Sanderson J, Roche K, Dell Acqua M, et al. Autonomous CaMKII mediates both LTP and LTD using a mechanism for differential substrate site selection. Cell Rep. 2014;6:431-7 pubmed publisher
    ..Thus, requirement of autonomous CaMKII in opposing forms of plasticity involves distinct substrate classes that are differentially regulated to enable stimulus-dependent substrate-site preference. ..
  8. Murphy J, Sanderson J, Gorski J, Scott J, Catterall W, Sather W, et al. AKAP-anchored PKA maintains neuronal L-type calcium channel activity and NFAT transcriptional signaling. Cell Rep. 2014;7:1577-1588 pubmed publisher
    ..Thus, LTCC-NFAT transcriptional signaling in neurons requires precise organization and balancing of PKA and CaN activities in the channel nanoenvironment, which is only made possible by AKAP79/150 scaffolding. ..
  9. Woolfrey K, Sanderson J, Dell Acqua M. The palmitoyl acyltransferase DHHC2 regulates recycling endosome exocytosis and synaptic potentiation through palmitoylation of AKAP79/150. J Neurosci. 2015;35:442-56 pubmed publisher
    ..Thus, we conclude that DHHC2-AKAP79/150 signaling is an essential regulator of dendritic recycling endosome exocytosis that controls both structural and functional plasticity at excitatory synapses. ..

More Information


  1. Sanderson J, Gorski J, Dell Acqua M. NMDA Receptor-Dependent LTD Requires Transient Synaptic Incorporation of Ca²⁺-Permeable AMPARs Mediated by AKAP150-Anchored PKA and Calcineurin. Neuron. 2016;89:1000-15 pubmed publisher
    ..Importantly, blocking CP-AMPAR recruitment, removal, or activity interferes with LTD. Thus, CP-AMPAR synaptic recruitment is required to transiently augment NMDAR Ca(2+) signaling during LTD induction. ..
  2. Dittmer P, Wild A, Dell Acqua M, Sather W. STIM1 Ca2+ Sensor Control of L-type Ca2+-Channel-Dependent Dendritic Spine Structural Plasticity and Nuclear Signaling. Cell Rep. 2017;19:321-334 pubmed publisher
    ..These findings of negative feedback control of LTCC signaling by STIM1 reveal interplay between Ca2+ influx and release from stores that controls both postsynaptic structural plasticity and downstream nuclear signaling. ..
  3. Sanderson J, Scott J, Dell Acqua M. Control of Homeostatic Synaptic Plasticity by AKAP-Anchored Kinase and Phosphatase Regulation of Ca2+-Permeable AMPA Receptors. J Neurosci. 2018;38:2863-2876 pubmed publisher
    ..These novel findings significantly expand our understanding of homeostatic plasticity mechanisms and further emphasize how intertwined they are with LTP and LTD. ..