anti-Dihydropyrimidinase-Like 2 (DPYSL2) Antikörper

Human Dihydropyrimidinase-Like 2 (DPYSL2) Interaktionspartner

1. cross-talk between distinct CRMP2 posttranslational modifications is a key factor in determining NaV1.7 trafficking and localization

2. crystal structure of human tetrameric CRMP-2

3. increased pCRMP2 may underlie the axonal pathology of Lewy body dementias.

4. These data identify a novel oncogenic mechanism where CDK5 activation induces CRMP2A phosphorylation in the nuclei of tumour cells

5. polymorphisms of the DPYSL2 gene in humans may be associated with the development of schizophrenia.

6. Functional variants in DPYSL2 sequence increase risk of schizophrenia and suggest a link to mTOR signaling

7. Changes for CRMP2, TCP1epsilon, TPM2 and 14-3-3gamma were confirmed in experimental tumors and in a series of 28 human SI-NETs.

8. Reduced CRMP2 expression and elevated expression of nuclear phosphorylated CRMP2 may be associated with breast cancer progression.

9. Levels of total GSK3 were decreased in the Huntington disease-affected frontal cortex and this correlated with decreased phosphorylated CRMP2.

10. High dihydropyrimidinase-related protein 2 expression is associated with lung cancer.

11. genetic variants in DPYSL2 may play a role in susceptibility to alcohol dependence.

12. 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.

13. 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.

14. a novel regulatory mechanism that utilizes CRMP2 SUMOylation to choreograph NaV1.7 trafficking.

15. a new insight into CRMP-2 as a controller of myosin II-mediated cellular functions through the inhibition of ROCK II in nonneuronal cells

16. No Alzheimer disease-associated differences in CNP and DPYSL2 promoter DNA methylation were observed.

17. 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.

18. High levels of nuclear phosphorylated CRMP-2 is associated with lung cancer.

19. CRMP2 hyperphosphorylation is speci fi c to Alzheimer's disease and is not a common event in all forms of dementia and neurodegeneration, especially other tauopathies.

20. findings suggest a major role of phosphorylated CRMP-2 as a mechanism involved in process retraction induced by reactive oxygen species

Zebrafish Dihydropyrimidinase-Like 2 (DPYSL2) Interaktionspartner

1. 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.

2. 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

3. 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.

4. 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.

Mouse (Murine) Dihydropyrimidinase-Like 2 (DPYSL2) Interaktionspartner

1. postulate that this state forces CRMP2 toward a monomer, exposing the SUMO site and consequently, resulting in constitutive regulation of NaV1.7.

2. 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.

3. The findings reveal a critical role for CRMP2 in neuronal plasticity, neural function and behavioral modulation in mice.

4. 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

5. 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.

6. 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.

7. study implies that dysregulation of CRMP2 may be involved in pathophysiology of neuropsychiatric disorders

8. 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.

9. We propose that CRMP2 could contribute to long-lasting synaptic plasticity.

10. 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

11. 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+

12. 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.

13. Glycogen synthase kinase 3beta has a role in microtubule remodeling in compensatory glomerular adaptation to podocyte depletion through Tau and CRMP2

14. Levels of total GSK3 were decreased in the Huntington disease-affected frontal cortex and this correlated with decreased phosphorylated CRMP2.

15. 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.

16. Noncanonical kainate receptor signaling influences neuronal development by modulating CRMP2 activity.

17. a novel regulatory mechanism that utilizes CRMP2 SUMOylation to choreograph NaV1.7 trafficking.

18. A novel glycogen synthase kinasealpha/beta CRMP-2 pathway is identified that connects neuronal activity to dendritic growth.

19. CRMP2 phosphorylation is critical for proper bifurcation of apical dendrite of CA1 pyramidal neurons

20. Two novel matrix metallopeptidase 9 targets were identified: synaptic cell adhesion molecule-2 and collapsin response mediator protein-2