CRMPs: critical molecules for neurite morphogenesis and neuropsychiatric diseases

Quach, Tam; Honnorat, Jérôme; Kolattukudy, P.E.; Khanna, Rajesh; Duchemin, Anne‐Marie

doi:10.1038/mp.2015.77

Cited by 92 publications

(96 citation statements)

References 131 publications

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“…1 and Quach et al . 2 ). Members of the CRMP family are reported to be involved in the pathogenesis of various neuronal disorders.…”

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confidence: 99%

“…1 The potential interplay between PTMs of CRMPs likely contributes to a ‘PTM code’ that pairs a particular PTM signature with a particular function. As expression and/or PTMs of CRMPs are altered in mental (schizophrenia and mood disorders) and neurological (Alzheimer's, prion encephalopathy, epilepsy and others) disorders, 2 it is likely that targeting these PTM codes may be a novel therapeutic strategy for neuropsychiatric disorders. Here, we illustrate the potential of such targeting applied to a chronic pain model.…”

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confidence: 99%

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Blocking CRMP2 SUMOylation reverses neuropathic pain

et al. 2017

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“…1 and Quach et al . 2 ). Members of the CRMP family are reported to be involved in the pathogenesis of various neuronal disorders.…”

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confidence: 99%

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Blocking CRMP2 SUMOylation reverses neuropathic pain

et al. 2017

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“…Expression patterns are characteristic in CRMPs1-5 and are dependent on the region it is expressed in, but uniform expression has been highly observed in the nervous system during the early postnatal stages to adulthood. For more information on the expression pattern of CRMPs, refer to the review [11]. Furthermore, homology is high (70-80 %) among the CRMPs1-4, which functions as a heterotetramer [17,18].…”

Section: Homology and Heterogeneity Of Crmpsmentioning

confidence: 99%

“…Taking into consideration the limited regenerative capacity of the CNS, the roles of CRMP in neuronal degeneration are described. For information on the relationship between CRMPs and Alzheimer's disease (AD), neuropsychiatric disease, and epilepsy, see other reviews [10,11]. Crmp1-/-Decrease in granule cell proliferation and apoptosis [45] Schizophrenia-like phenotype [47] Retarded neuronal migration [49] Disorientation of apical dendrites and impaired dendritic spine density [48] Impaired learning and memory [46,47] CRMP2…”

Section: Crmps In Neuronal Degeneration and Regenerationmentioning

confidence: 99%

“…For additional details about the following topics, readers may refer to several outstanding reviews: CRMPs phosphorylation in neural development [8], roles of CRMPs in neuronal polarity during cortical migration [9], CRMP2 in neurological diseases [10], and the expression pattern and potential involvement of CRMPs in human neuropsychiatric diseases [11].…”

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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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Microtubule and microtubule associated protein anomalies in psychiatric disease

2016

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Anomalies in neuronal cell architecture, in particular dendritic complexity and synaptic density changes, are widely observed in the brains of subjects with schizophrenia or mood disorders. The concept that a disturbed microtubule cytoskeleton underlies these abnormalities and disrupts synaptic connectivity is supported by evidence from clinical studies and animal models. Prominent changes in tubulin expression levels are commonly found in disease specific regions such as the hippocampus and prefrontal cortex of psychiatric patients. Genetic linkage studies associate tubulinbinding proteins such as the dihydropyrimidinase family with an increased risk to develop schizophrenia and bipolar disorder. For many years, altered immunoreactivity of microtubule associated protein-2 has been a hallmark found in the brains of individuals with schizophrenia. In this review, we present a growing body of evidence that connects a dysfunctional microtubule cytoskeleton with neuropsychiatric illnesses. Findings from animal models are discussed together with clinical data with a particular focus on tubulin posttranslational modifications and on microtubule-binding proteins. V C 2016 Wiley Periodicals, Inc.Key Words: microtubule; depression; schizophrenia; MAP2; JNK Introduction I t is almost 50 years since tubulin was identified as the globular protein that makes up microtubules [Mohri, 1968]. Tubulin polymers, or microtubules, along with actin microfilaments and intermediate filaments, make up the cytoskeletal framework, which provides structure and dynamics to cells [Wells, 2005]. Neuronal cells are exceptional in their usage of microtubules to generate a highly polarized morphology consisting of long axons and dendritic arbors that form the receptive field for electrochemical input. Axonal microtubules are polarized and confer the rigidity that is necessary for long distance transport, whereas dendritic microtubules show mixed polarity and influence processes such as arborization and signaling to dendritic spines .In cells, a and b tubulin exist as heterodimers. They are structurally homologous, comprising two b-strands surrounded by a-helices. Each subunit is divided into three functional domains: the N-terminal domain that incorporates a nucleotide-binding region (i.e., GTP), an intermediate domain comprising the taxol-binding site, and a Cterminal domain which provides the binding surface for motor proteins [Nogales et al., 1998]. a/b heterodimers interact in a head-to-tail conformation giving rise to linear polymers with inherent polarity known as protofilaments [Black and Baas, 1989]. Typically, a microtubule consists of a cylindrical assembly of 13 protofilaments with a diameter of 25 nm, and highly variable length. Microtubules actively modify their structure through dynamic cycles of assembly and disassembly. The plus end where b-tubulin is exposed elongates more rapidly than the a-tubulin exposed, minus end [Horio et al., 2014]. The process of rapid growth and collapse of microtubules is known as dynamic instability a...

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CRMPs: critical molecules for neurite morphogenesis and neuropsychiatric diseases

Cited by 92 publications

References 131 publications

Blocking CRMP2 SUMOylation reverses neuropathic pain

Blocking CRMP2 SUMOylation reverses neuropathic pain

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

Microtubule and microtubule associated protein anomalies in psychiatric disease

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