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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 08 Dec 2016.

Dihydropyrimidinase-like 4

CRMP3, Ulip4, collapsin response mediator protein-3, DRP-4
protein that may regulate neuronal plasticity by transducing signals from semaphorins [RGD, Feb 2006] (from NCBI)
Papers on CRMP3
Identification of dihydropyrimidinase-related protein 4 as a novel target of the p53 tumor suppressor in the apoptotic response to DNA damage.
Yoshida et al., Tokyo, Japan. In Int J Cancer, 2011
DPYSL4 is a novel apoptosis-inducible factor controlled by p53 in response to DNA damage
Characterization of the role of full-length CRMP3 and its calpain-cleaved product in inhibiting microtubule polymerization and neurite outgrowth.
Hou et al., Ottawa, Canada. In Exp Cell Res, 2009
Data show CRMP3's role in attenuating neurite outgrowth possibility through inhibiting microtubule polymerization, and also reveal its novel association with vimentin during nuclear condensation prior to neuronal death.
Calpain-truncated CRMP-3 and -4 contribute to potassium deprivation-induced apoptosis of cerebellar granule neurons.
Li et al., Guangzhou, China. In Proteomics, 2009
The findings demonstrated that calpain-truncated CRMP-3 and -4 act as pro-apoptotic players when CGNs undergo apoptosis.
CRMP3 is required for hippocampal CA1 dendritic organization and plasticity.
Kolattukudy et al., Lyon, France. In Faseb J, 2008
indicate an important role for CRMP3 in dendrite arborization, guide-posts navigation, and neuronal plasticity
Calpain-cleaved collapsin response mediator protein-3 induces neuronal death after glutamate toxicity and cerebral ischemia.
Kappler et al., Ottawa, Canada. In J Neurosci, 2006
Collectively, these results reveal a novel role of CRMP-3 in that calpain cleavage of CRMP-3 and the subsequent nuclear translocation of the truncated CRMP-3 evokes neuronal death in response to excitotoxicity and cerebral ischemia.
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