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To evaluate the role of CRMP2 phosphorylation in amyotrophic lateral sclerosis pathogenesis, we utilized CRMP2 S522A knock-in (CRMP2(ki/ki)) mice, in which the serine residue 522 was homozygously replaced with alanine and thereby making CRMP2 no longer phosphorylatable by CDK5 or GSK3B
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suppression of CRMP2 phosphorylation may be a novel therapeutic target for Parkinson's disease.
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Results show that collapsin response mediator protein 2 is required for platelet derived growth factor-directed cell migration in vitro.
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postulate that this state forces CRMP2 toward a monomer, exposing the SUMO site and consequently, resulting in constitutive regulation of NaV1.7.
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These results revealed that bilateral ligation of the internal carotid artery causes retinal ischemia in mice. Moreover, CRMP2 might play a pivotal role during the ischemic injury in the retina and inhibit the cleavage of CRMP2 can ameliorate the IH injury.
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The findings reveal a critical role for CRMP2 in neuronal plasticity, neural function and behavioral modulation in mice.
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Results suggested that crmp2 is a target of miR-181c and that the abnormally low expression of miR-181c in the hippocampus of SAMP8 mice could lead to an increase of the crmp2 protein level in Alzheimer's disease mice, which might potentially play a role in the pathogenesis of Alzheimer's disease
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These results suggest a correlation between CRMP2 phosphorylation and AD pathophysiology, and indicate the effectiveness of pioglitazone treatment at the pre-Abeta accumulation stage in AD model mice.
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We generated CRMP2 gene-deficient (crmp2(-/-) ) mice. The crmp2(-/-) mice showed irregular development of dendritic spines in cortical neurons. The level of CRMP1 was increased in crmp2(-/-) , but the level of CRMP2 was not altered in crmp1(-/-).The phenotypic defects had no genetic interaction between crmp1 and crmp2.
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study implies that dysregulation of CRMP2 may be involved in pathophysiology of neuropsychiatric disorders
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we demonstrate that Cdk5 phosphorylates collapsin response mediator protein 2 (CRMP2) in the dendritic spines of cultured hippocampal neurons and in vivo in the mouse brain. When we eliminated CRMP2 phosphorylation in CRMP2(KI/KI) mice, the densities of dendritic spines significantly decreased in hippocampal CA1 pyramidal neurons in the mouse brain.
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We propose that CRMP2 could contribute to long-lasting synaptic plasticity.
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This study shows that in young adult mice, motor and sensory functions lost by SCI can be recovered with a single genetic mutation to inhibit CRMP2 phosphorylation
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Study showed that axon degeneration is an early and dominant feature in dopaminergic neurons treated with 1-methyl-4-phenylpyridiniumion (MPP+), and that the Akt/GSK-3beta/CRMP-2 pathway is involved in axon degeneration induced by MPP+
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Clear differences in CRMP2 protein abundance and degradation product/short isoform were observed between ischemic core and penumbra and also compared to the contralateral healthy tissues after PACAP38 or saline treatment.
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Glycogen synthase kinase 3beta has a role in microtubule remodeling in compensatory glomerular adaptation to podocyte depletion through Tau and CRMP2
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Levels of total GSK3 were decreased in the Huntington disease-affected frontal cortex and this correlated with decreased phosphorylated CRMP2.
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Long-term vitamin E-deficiency led to significantly increased expression of the phosphorylated form of collapsin response mediator protein (CRMP)-2 compared to short-term deficiency.
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Noncanonical kainate receptor signaling influences neuronal development by modulating CRMP2 activity.
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a novel regulatory mechanism that utilizes CRMP2 SUMOylation to choreograph NaV1.7 trafficking.
