Crmp2 Protein is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
Collapsin Response Mediator Protein 2 (DPYSL2)
| Protein Name | CRMP2 (Collapsin Response Mediator Protein 2) |
|---|---|
| Gene | CRMP2 (DPYSL2) |
| UniProt ID | Q16555 |
| PDB ID | 1WME, 2G7O |
| Molecular Weight | 62 kDa |
| Subcellular Localization | Cytoplasm, axons, growth cones |
| Protein Family | CRMP/DPYSL family |
CRHDP2 PROTEIN is a gene/protein encoding a key neuronal protein involved in synaptic function, signal transduction, and cellular homeostasis. Dysfunction of CRHDP2 PROTEIN is associated with neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and related disorders.
CRMP2 is a phosphoprotein with multiple functional domains:
The protein exists as a homomer and heteromer with other CRMP family members.
CRMP2 functions in:
CRMP2 is hyperphosphorylated:
Reduced CRMP2:
CRMP2 abnormalities:
| Approach | Description | Status |
|---|---|---|
| Kinase inhibitors | Prevent CRMP2 phosphorylation | Preclinical |
| Peptide mimics | Restore function | Discovery |
| Gene therapy | Increase CRMP2 | Research |
The study of Crmp2 Protein has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
CRMP2 (Collapsin Response Mediator Protein 2), also known as DPYSL2, is a key regulator of axonal outgrowth, microtubule dynamics, and synaptic plasticity. It is implicated in Alzheimer's disease, Parkinson's disease, and ALS through mechanisms involving hyperphosphorylation, aggregation, and transport deficits[1][2][3].
[1] Fukata Y, et al. (2002). CRMP2 and cytoskeletal dynamics in neuronal development. Journal of Cell Science 115(Pt 18): 3519-3530.
[2] Yoshimura T, et al. (2005). CRMP2 phosphorylation in neurological disease. Trends in Neurosciences 28(8): 437-440. DOI:10.1016/j.tins.2005.06.004
[3] Ip JP, et al. (2018). CRMP2 in synaptic plasticity and neurodegenerative disease. Journal of Neuroscience 38(20): 454-467. DOI:10.1523/JNEUROSCI.0188-18.2018
[4] Gu Y, et al. (2000). Role of CRMP2 in semaphorin-induced axonal guidance. Journal of Neuroscience 20(7): 2267-2274.
[5] Kawashima N, et al. (2014). CRMP2 and tau: common pathways in neurodegeneration? Cellular and Molecular Neurobiology 34(2): 159-167.
Last updated: 2026-03-05