Activity-Dependent Modulation of the Interaction between CaMKIIα and Abi1 and Its Involvement in Spine Maturation

Park, Esther; Chi, Susan; Park, Dongeun

doi:10.1523/jneurosci.2257-12.2012

Cited by 15 publications

(17 citation statements)

References 35 publications

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“…Calpain-5 is a non-classical member of the calpain family that is highly expressed in the CNS [49], but whether it functions the same way as the other members in synaptic activity and neurotoxixity is unknown. Some proteins are associated with neurite extension/synapse maturation or neuronal viability during neural development (Abl interactor [50,51], gamma-adducin [52,53], FKBP8 [54,55], hippocalcin [56,57], CD47 [58], Nova-1 [59,60], TANC2 [61] and Teneurin [62,63]). And several listed proteins have been reported to participate in cell death mechanisms in adult brain ischemia (Dynamin-1 [64,65], FKBP8 [66], CD47 [67,68] and TDP-43 [69,70]).…”

Section: Resultsmentioning

confidence: 99%

Proteomic Analysis of Mouse Cortex Postsynaptic Density following Neonatal Brain Hypoxia-Ischemia

Shao

Wang²,

Guan³

et al. 2017

Dev Neurosci

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Proteomics of the synapses and postsynaptic densities (PSDs) have provided a deep understanding of protein composition and signal networks in the adult brain, which underlie neuronal plasticity and neurodegenerative or psychiatric disorders. However, there is a paucity of knowledge about the architecture and organization of PSDs in the immature brain, and how it is modified by brain injury in an early developing stage. Mass spectrometry (MS)-based proteomic analysis was performed on PSDs prepared from cortices of postnatal day 9 naïve mice or pups which had suffered hypoxic-ischemic (HI) brain injury. 512 proteins of different functional groups were identified from PSDs collected 1 h after HI injury, among which 60 have not been reported previously. Seven newly identified proteins involved in neural development were highlighted. HI injury increased the yield of PSDs at early time points upon reperfusion, and multiple proteins were recruited into PSDs following the insult. Quantitative analysis was performed using spectral counting, and proteins whose relative expression was more than 50% up- or downregulated compared to the sham animals 1 h after HI insult were reported. Validation with Western blotting demonstrated changes in expression and phosphorylation of the N-methyl-D-aspartate receptor, activation of a series of postsynaptic protein kinases and dysregulation of scaffold and adaptor proteins in response to neonatal HI insult. This work, along with other recent studies of synaptic protein profiling in the immature brain, builds a foundation for future investigation on the molecular mechanisms underlying developing plasticity. Furthermore, it provides insights into the biochemical changes of PSDs following early brain hypoxia-ischemia, which is helpful for understanding not only the injury mechanisms, but also the process of repair or replenishment of neuronal circuits during recovery from brain damage.

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Section: Resultsmentioning

confidence: 99%

Proteomic Analysis of Mouse Cortex Postsynaptic Density following Neonatal Brain Hypoxia-Ischemia

Shao

Wang²,

Guan³

et al. 2017

Dev Neurosci

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“…The mutants were verified by automated DNA sequencing. We used a GST-PBD construct described previously (Park et al, 2012). GST-Rac1G15A construct was a kind gift from J. G. Hanley (University of Bristol, Bristol, UK).…”

Section: Dna Constructsmentioning

confidence: 99%

“…Dissociated hippocampal (for staining experiments) and cortical (for biochemical experiments) neurons were prepared from embryonic day 18 (E18) Sprague-Dawley rat embryos and postnatal day 0 (P0) pups of neuronspecific βPix isoform KO mice of either sex as described previously (Beaudoin et al, 2012;Park et al, 2012). We used protocols described in Park et al (2012) and Beaudoin et al (2012) for neuron cultures, with minor modifications. In brief, dissociated hippocampal and cortex tissues were treated with papain (20 µg/ml, Worthington) and DNase (10 U/µl, Sigma-Aldrich) for 25 min at 37°C.…”

Section: Primary Neuronal Culture and Transfectionmentioning

confidence: 99%

Src-mediated phosphorylation of βPix-b regulates dendritic spine morphogenesis

Shin

Song

Shin

et al. 2019

Journal of Cell Science

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PAK-interacting guanine nucleotide exchange factor (βPix; also known as Arhgef7) has been implicated in many actin-based cellular processes, including spine morphogenesis in neurons. However, the molecular mechanisms by which βPix controls spine morphology remain elusive. Previously, we have reported the expression of several alternative spliced βPix isoforms in the brain. Here, we report a novel finding that the b isoform of βPix (βPix-b) mediates the regulation of spine and synapse formation. We found that βPix-b, which is mainly expressed in neurons, enhances spine and synapse formation through preferential localization at spines. In neurons, glutamate treatment efficiently stimulates Rac1 GEF activity of βPix-b. The glutamate stimulation also promotes Src-mediated phosphorylation of βPix-b in both an AMPA receptor-and NMDA receptor-dependent manner. Tyrosine 598 (Y598) of βPix-b is identified as the major Src-mediated phosphorylation site. Finally, Y598 phosphorylation of βPix-b enhances its Rac1 GEF activity that is critical for spine and synapse formation. In conclusion, we provide a novel mechanism by which βPix-b regulates activity-dependent spinogenesis and synaptogenesis via Src-mediated phosphorylation.

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“…Interestingly, it has been shown in hippocampal neurons that, similar to knockout of the Arp2/3 complex, small interfering RNA (siRNA) knockdown of cortactin results in decreased dendritic spine density [10]. Abelson interactor 1 (Abi1) is an adaptor protein that binds the Wiskott–Aldrich syndrome protein (WASP)-family verprolin homologous protein 1 (WAVE1) and is critical for neurotypical dendritic spine morphology through interaction with Ca 2+ /calmodulin-dependent kinase IIα [11, 12]. …”

Section: Introductionmentioning

confidence: 99%

Decreased expression of cortactin in the schizophrenia brain

et al. 2016

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Schizophrenia is a severe psychiatric disorder that is characterized by a wide array of symptoms and complex neuropathology. A well-characterized neurobiological feature of schizophrenia is abnormal synaptic plasticity, although the mechanisms underlying this are not fully understood. Numerous studies have demonstrated a link between proper functioning of the cytoskeleton and synaptic plasticity. The Arp2/3 complex is responsible for the nucleation of new actin filaments and elongation of existing actin filaments and is thus crucial to cytoskeletal dynamics, especially actin polymerization and organization. To determine if the Arp2/3 complex is abnormally expressed in schizophrenia, we measured the protein expression of Arp2 and Arp3, as well as Arp2/3 complex binding partners and associated proteins including cortactin, N-WASP, WAVE1, and Abi1 in superior temporal gyrus of paired schizophrenia and comparison subjects. No changes were found in Arp2, Arp3, N-WASP, WAVE1, or Abi1. However, all three isoforms of cortactin were decreased in schizophrenia. Specifically, the 62 kDa isoform was decreased 43%; the 71kDa isoform was decreased 32%; and the 58 kDa isoform was decreased 35%. Cortactin regulates branching of filamentous actin via its binding and activation of the Arp2/3 complex and is thus critical to the formation of stable actin networks. These findings contribute to a growing body of evidence implicating altered cytoskeletal dynamics in schizophrenia.

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Activity-Dependent Modulation of the Interaction between CaMKIIα and Abi1 and Its Involvement in Spine Maturation

Cited by 15 publications

References 35 publications

Proteomic Analysis of Mouse Cortex Postsynaptic Density following Neonatal Brain Hypoxia-Ischemia

Proteomic Analysis of Mouse Cortex Postsynaptic Density following Neonatal Brain Hypoxia-Ischemia

Src-mediated phosphorylation of βPix-b regulates dendritic spine morphogenesis

Decreased expression of cortactin in the schizophrenia brain

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