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Human Monoclonal DPYSL2 Primary Antibody for IHC (p), WB - ABIN4300547
Xu, Wicki-Stordeur, Sanchez-Arias, Liu, Weaver, Choi, Swayne: Probenecid Disrupts a Novel Pannexin 1-Collapsin Response Mediator Protein 2 Interaction and Increases Microtubule Stability. in Frontiers in cellular neuroscience 2018
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Human Polyclonal DPYSL2 Primary Antibody for IF (p), IHC (p) - ABIN734468
Zheng, Liu, Li, Tang, Zhang, Tang: Lithium posttreatment confers neuroprotection through glycogen synthase kinase-3β inhibition in intracerebral hemorrhage rats. in Journal of neurosurgery 2016
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Human Polyclonal DPYSL2 Primary Antibody for IF (p), IHC (p) - ABIN683668
Guo, Zhao, Ming, Hong, Liu, Li: Sumatriptan inhibits the electrophysiological activity of ASICs in rat trigeminal ganglion neurons. in European journal of pharmacology 2019
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Human Monoclonal DPYSL2 Primary Antibody for IF, ELISA - ABIN515065
OBrien, Shen, Tachikawa, Lee, Briggs: Quantitative proteome analysis of pluripotent cells by iTRAQ mass tagging reveals post-transcriptional regulation of proteins required for ES cell self-renewal. in Molecular & cellular proteomics : MCP 2010
Human Polyclonal DPYSL2 Primary Antibody for IHC - ABIN966010
Goshima, Nakamura, Strittmatter, Strittmatter: Collapsin-induced growth cone collapse mediated by an intracellular protein related to UNC-33. in Nature 1995
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The interaction between Prx2 and CRMP2 is conserved among humans and rodents.
It demonstrates the enzyme/substrate nature of Ubc9/CRMP2 binding and identify hot spots on CRMP2 that may form the basis of future drug discovery campaigns disrupting the CRMP2-Ubc9 interaction to recapitulate allosteric regulation of NaV1.7 for pain relief.
These results introduce CRMP2 expression and phosphorylation as a novel player in glioblastoma proliferation and survival.
cross-talk between distinct CRMP2 posttranslational modifications is a key factor in determining NaV1.7 trafficking and localization
crystal structure of human tetrameric CRMP-2
increased pCRMP2 may underlie the axonal pathology of Lewy body dementias.
These data identify a novel oncogenic mechanism where CDK5 activation induces CRMP2A phosphorylation in the nuclei of tumour cells
polymorphisms of the DPYSL2 gene in humans may be associated with the development of schizophrenia.
Functional variants in DPYSL2 sequence increase risk of schizophrenia and suggest a link to mTOR signaling
Changes for CRMP2, TCP1epsilon, TPM2 and 14-3-3gamma were confirmed in experimental tumors and in a series of 28 human SI-NETs.
Reduced CRMP2 expression and elevated expression of nuclear phosphorylated CRMP2 may be associated with breast cancer progression.
Levels of total GSK3 were decreased in the Huntington disease-affected frontal cortex and this correlated with decreased phosphorylated CRMP2.
High dihydropyrimidinase-related protein 2 expression is associated with lung cancer.
genetic variants in DPYSL2 may play a role in susceptibility to alcohol dependence.
A specific and reversible intermolecular Cys-504-Cys-504 dithiol-disulfide switch in homotetrameric CRMP2 determines two conformations of the quaternary CRMP2 complex that controls axonal outgrowth and thus neuronal development.
CRMP-2-dependent regulation of ROCK II activity is mediated through interaction of the CRMP-2L N terminus with the ROCK II catalytic domain as well as by GSK3-dependent phosphorylation of CRMP-2.
a novel regulatory mechanism that utilizes CRMP2 SUMOylation to choreograph NaV1.7 trafficking.
a new insight into CRMP-2 as a controller of myosin II-mediated cellular functions through the inhibition of ROCK II in nonneuronal cells
No Alzheimer disease-associated differences in CNP and DPYSL2 promoter DNA methylation were observed.
Deletion analysis of CRMP-2 identified a 51 amino acid sequence in the C-terminus that is required for targeting to the basal body and primary cilium. This domain contains GSK-3beta phosphorylation sites.
Results demonstrate that collapsin response mediator proteins 2 and 4 function differentially in axon development and are required for axon guidance and growth in zebrafish retinal neurons.
phosphorylation of Dpysl2 and Dpysl3 by Cyclin-dependent kinase 5 and dual-specificity tyrosine-phosphorylated and regulated kinase 2 is required for correct positioning of CaP motor neurons in the zebrafish spinal cord
These results suggest that the phosphorylation of Dpysl2 and Dpysl3 by Cdk5 and DYRK2 is required for the proper positioning of Rohon-Beard neurons and neural crest cells during neurulation in zebrafish embryos.
From 20 somites through 30 hpf CRMP2 is expressed in the dorsal rostral cluster of the telencephalon, the ventral rostral cluster of the diencephalon, the ventral caudal cluster of the mesencephalon, and the hindbrain clusters.
our results suggest that proper control of TGF-beta/Smads/CRMP2 signaling pathways is critical for the precise execution of neuronal morphogenesis, whose impairment eventually results in neurodevelopmental disorders
that the phosphorylation of CRMP2 at Ser522 is involved in the signaling pathways that may be related to neuropsychiatric and neurodegenerative diseases and pain
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
suppression of CRMP2 phosphorylation may be a novel therapeutic target for Parkinson's disease.
Results show that collapsin response mediator protein 2 is required for platelet derived growth factor-directed cell migration in vitro.
postulate that this state forces CRMP2 toward a monomer, exposing the SUMO site and consequently, resulting in constitutive regulation of NaV1.7.
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.
The findings reveal a critical role for CRMP2 in neuronal plasticity, neural function and behavioral modulation in mice.
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
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.
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.
study implies that dysregulation of CRMP2 may be involved in pathophysiology of neuropsychiatric disorders
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.
We propose that CRMP2 could contribute to long-lasting synaptic plasticity.
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
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+
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.
Glycogen synthase kinase 3beta has a role in microtubule remodeling in compensatory glomerular adaptation to podocyte depletion through Tau and CRMP2
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.
This gene encodes a member of the collapsin response mediator protein family. Collapsin response mediator proteins form homo- and hetero-tetramers and facilitate neuron guidance, growth and polarity. The encoded protein promotes microtubule assembly and is required for Sema3A-mediated growth cone collapse, and also plays a role in synaptic signaling through interactions with calcium channels. This gene has been implicated in multiple neurological disorders, and hyperphosphorylation of the encoded protein may play a key role in the development of Alzheimer's disease. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
collapsin response mediator protein hCRMP-2
, dihydropyrimidinase-related protein 2
, unc-33-like phosphoprotein 2
, collapsin response mediator protein 2
, neural-specific protein NSP60
, turned on after division 64
, dihydropyrimidinase-like 2
, turned on after division 64 kDa protein
, turned on after division, 64 kDa protein
, collapsin response mediator protein CRMP-62
, collapsin response mediator protein-2A
, dihydropyrimidinase-related protein 2-like