Phosphorylation of CRMP2 (Collapsin Response Mediator Protein 2) Is Involved in Proper Dendritic Field Organization

Yamashita, Naoya; Ohshima, Toshio; Nakamura, Fumio; Kolattukudy, P.E.; Honnorat, Jérôme; Mikoshiba, Katsuhiko; Goshima, Yoshio

doi:10.1523/jneurosci.5563-11.2012

Cited by 88 publications

(88 citation statements)

References 28 publications

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“…Crmp2KI/KI mice displayed a reduction in spine density [50], supporting the notion of CRMP2 functioning as substrate of Cdk5, since a decrease in the number of synapses of hippocampal neurons was observed in mice lacking Cdk5 activity [51,52]. Moreover, Crmp1−/− and Crmp2KI/KI double mutants displayed a more severe abnormality in the dendritic organization of layer V cortical neurons in comparison to Crmp1−/− single mutants [53]. Furthermore, abnormal hippocampal dendritic organization and spine formation in Crmp3−/− mice led to irregularities in long-term potentiation (LTP) and PPI [54,55].…”

Section: Crmps In Neural Circuit Formationsupporting

confidence: 62%

“…CRMP double mutants have a severe phenotype [53,62]. Due to the redundancy that occurs between CRMPs, analyses of mice with multiple genetic modifications would be insightful.…”

Section: Crmps In Neural Circuit Formationmentioning

confidence: 99%

“…Crmp2KI/KI* Reduced spine density [51] Motor and sensory recovery with axon growth after SCI [42] Severely abnormal dendritic patterning (Crmp1−/− background) [53] Reduced inflammation and scar formation [42] Increased proximal bifurcation…”

Section: Crmps In Neuronal Degeneration and Regenerationmentioning

confidence: 99%

“…Therefore, because CRMPs are highly expressed in the nervous system, therapeutic treatments that can target CRMPs directly are more clinically relevant [8]. As a matter of fact, Crmp gene mutant mice did not exhibit any gross alterations in their body growth or fertility [53,62], while mutant mice lacking Sema3a, Cdk5, Gsk3β, or Rock gene expressed embryonic lethality [118][119][120][121].…”

Section: Crmps In Inflammatory Cellsmentioning

confidence: 99%

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CRMPs Function in Neurons and Glial Cells: Potential Therapeutic Targets for Neurodegenerative Diseases and CNS Injury

2016

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Neurodegeneration in the adult mammalian central nervous system (CNS) is fundamentally accelerated by its intrinsic neuronal mechanisms, including its poor regenerative capacity and potent extrinsic inhibitory factors. Thus, the treatment of neurodegenerative diseases faces many obstacles. The degenerative processes, consisting of axonal/dendritic structural disruption, abnormal axonal transport, release of extracellular factors, and inflammation, are often controlled by the cytoskeleton. From this perspective, regulators of the cytoskeleton could potentially be a therapeutic target for neurodegenerative diseases and CNS injury. Collapsin response mediator proteins (CRMPs) are known to regulate the assembly of cytoskeletal proteins in neurons, as well as control axonal growth and neural circuit formation. Recent studies have provided some novel insights into the roles of CRMPs in several inhibitory signaling pathways of neurodegeneration, in addition to its functions in neurological disorders and CNS repair. Here, we summarize the roles of CRMPs in axon regeneration and its emerging functions in non-neuronal cells, especially in inflammatory responses. We also discuss the direct and indirect targeting of CRMPs as a novel therapeutic strategy for neurological diseases.

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Section: Crmps In Neural Circuit Formationsupporting

confidence: 62%

“…CRMP double mutants have a severe phenotype [53,62]. Due to the redundancy that occurs between CRMPs, analyses of mice with multiple genetic modifications would be insightful.…”

Section: Crmps In Neural Circuit Formationmentioning

confidence: 99%

Section: Crmps In Neuronal Degeneration and Regenerationmentioning

confidence: 99%

Section: Crmps In Inflammatory Cellsmentioning

confidence: 99%

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CRMPs Function in Neurons and Glial Cells: Potential Therapeutic Targets for Neurodegenerative Diseases and CNS Injury

2016

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“…20 Phosphorylated CRMP1 and CRMP2 are localized in the dendrites of cortical neurons where they regulate dendritic branch trajectories. 38 Mice with abnormal phosphorylation of CRMP1 and CRMP2 present a curling dendrite phenotype, 38 suggesting that these two molecules are critical for normal dendrite patterning in cortical neurons.…”

Section: Crmps Influence Neurite Initiation and Dendritic Outgrowthmentioning

confidence: 99%

CRMPs: critical molecules for neurite morphogenesis and neuropsychiatric diseases

et al. 2015

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Neuronal polarity and spatial rearrangement of neuronal processes are central to the development of all mature nervous systems. Recent studies have highlighted the dynamic expression of Collapsin-Response-Mediator Proteins (CRMPs) in neuronal dendritic/axonal compartments, described their interaction with cytoskeleton proteins, identified their ability to activate L- and N-type voltage-gated calcium channels (VGCCs) and delineated their crucial role as signaling molecules essential for neuron differentiation and neural network development and maintenance. In addition, evidence obtained from genome-wide/genetic linkage/proteomic/translational approaches revealed that CRMP expression is altered in human pathologies including mental (schizophrenia and mood disorders) and neurological (Alzheimer's, prion encephalopathy, epilepsy and others) disorders. Changes in CRMPs levels have been observed after psychotropic treatments, and disrupting CRMP2 binding to calcium channels blocked neuropathic pain. These observations, altogether with those obtained from genetically modified mice targeting individual CRMPs and RNA interference approaches, pave the way for considering CRMPs as potential early disease markers and modulation of their activity as therapeutic strategy for disorders associated with neurite abnormalities.

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Cellular and molecular mechanisms regulating neuronal growth by brain‐derived neurotrophic factor

et al. 2016

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Brain-derived neurotrophic factor (BDNF) and its receptors TrkB and p75 regulate dendritic and axonal growth during development and maintenance of the mature nervous system; however, the cellular and molecular mechanisms underlying this process are not fully understood. In recent years, several advances have shed new light on the processes behind the regulation of BDNF-mediated structural plasticity including control of neuronal transcription, local translation of proteins, and regulation of cytoskeleton and membrane dynamics. In this review, we summarize recent advances in the field of BDNF signaling in neurons to induce neuronal growth. V C 2016 Wiley Periodicals, Inc.Key Words: BDNF; dendritic growth; signaling; cytoskeleton dynamics; membrane trafficking Introduction T he functionality of the nervous system (NS) depends on the extent of connectivity achieved by neurons. Although there is wide range of neuronal morphologies, neurons are specialized to form part of a given neuronal circuit and thus their morphology must adjust to this task [Gao, 2007]. In this regard, neurons are highly polarized cells composed of two main domains: the somato-dendritic compartment where neurons receive and integrate information from several axonal inputs and axons that are responsible for transmitting the action potential and conveying the information to the next relay in the network. A close relationship between the appropriate development of dendrites and axons and the functionality of the NS has been described. For example, alterations in dendrites, axonal inputs and dendritic spines are linked to neurodevelopmental and neuropathological conditions. Thus, the study of the mechanisms implicated in the regulation of neuronal morphology during development and maintenance of the adult NS is a focus of intense research [Armstrong et al., 1998;Wood et al., 2004;Bronfman et al., 2007;Dickstein et al., 2010;Cabeza et al., 2012;Eiland and McEwen, 2012;Kulkarni and Firestein, 2012].Neuronal morphology is regulated by both intrinsic and extrinsic factors, whose actions are overlapping. The intrinsic factors are described as the action of the genetic program of neurons that leads to a basic pattern of branching. In addition to this, there is an extensive list of molecules grouped as extrinsic factors that shape axonal and dendritic morphology throughout development and in response to sensory experience. These include bone morphogenetic family proteins (BMPs), semaphorins, Reelin, neurotrophins, and neuronal activity, among others [Jan and Jan, 2010]. The mechanisms underlying the effects of external cues to induce dendritic and axonal branching have only begun to be understood, and several steps including stimulation of intracellular signaling pathways to activate specific transcription factors, local synthesis of proteins and cellular membrane addition and turnover are involved. An interesting point of convergence is the effect of these external signals on the stability and dynamics of the cytoskeleton and the activity of molecular mo...

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Phosphorylation of CRMP2 (Collapsin Response Mediator Protein 2) Is Involved in Proper Dendritic Field Organization

Cited by 88 publications

References 28 publications

CRMPs Function in Neurons and Glial Cells: Potential Therapeutic Targets for Neurodegenerative Diseases and CNS Injury

CRMPs Function in Neurons and Glial Cells: Potential Therapeutic Targets for Neurodegenerative Diseases and CNS Injury

CRMPs: critical molecules for neurite morphogenesis and neuropsychiatric diseases

Cellular and molecular mechanisms regulating neuronal growth by brain‐derived neurotrophic factor

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