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Data show that SRY-box containing gene 5 protein (Sox5) can physically bind to the collapsin response mediator protein 5 (CRMP5) promoter DNA.
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study elucidates a novel regulatory mechanism that utilizes CRMP5-induced mitophagy to orchestrate proper dendrite outgrowth and neuronal function.
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CRMP5-deficient mice show abnormal Schwann process extension resulting in abnormal cell-axon segregation, indicating that CRMP5 is involved in the morphologic adaptation of Schwann cells to surround axons.
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These findings provide the first evidence that CRMP5 is involved in the generation and survival of newly generated neurons in areas of the adult brain with a high level of activity-dependent neuronal plasticity.
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Data show that CRMP5 is involved in the development, maintenance and synaptic plasticity of Purkinje cells.
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The CRMP5 binding to tubulin modulates CRMP2 regulation of neurite outgrowth and neuronal polarity during brain development.
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CRAM regulates filopodial dynamics and growth cone development, thereby restricting the response of growth cone to repulsive guidance cues
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beyond their signalling function in axon outgrowth and guidance, CRMPs also play a role in mature neurons both in axons and in dendrites
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In the olfactory bulb, CRMP1, CRMP2 and CRMP5 are abundant in neuronal progenitors of the subependymal layer and in differentiating interneurons.
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Our results are therefore consistent with a role for CRMP5 in neuronal process extension.We conclude that expression of CRMP5 is consistent with a dynamic implicit role in forebrain development.
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Hypoxia-ischemia (HI)induces dephosphorylation of CRMPs (CRMP1, 2, and 5) in neonatal brain. Hypophosphorylated CRMPs might be implicated in the pathogenesis of HI-related neurological disorders.