CRMP2 (Collapsin Response Mediator Protein 2), also known as DPYSL2 or ULIP2. is a cytosolic phosphoprotein predominantly expressed in the nervous system. It belongs to the CRMP family, which comprises five isoforms (CRMP1-5) involved in neuronal development, axon guidance, and synaptic plasticity. CRMP2 plays a critical role in regulating microtubule dynamics, neurite outgrowth, and neurotransmitter release by interacting with tubulin heterodimers, kinases, and synaptic vesicle proteins. Its activity is modulated by post-translational modifications, particularly phosphorylation by kinases like GSK-3β and Cdk5. which influence its functional states.
CRMP2 antibodies are widely used as research tools to detect and study the protein's expression, localization, and interactions in both physiological and pathological contexts. Dysregulation of CRMP2 has been implicated in neurological disorders, including Alzheimer’s disease, epilepsy, neuropathic pain, and spinal cord injury. For instance, hyperphosphorylated CRMP2 is associated with amyloid-beta toxicity in Alzheimer’s models, while its cleavage by calpain contributes to axonal degeneration post-injury.
In therapeutic research, CRMP2 antibodies help validate its role as a biomarker or drug target. Small molecules like lacosamide (an antiepileptic) are known to modulate CRMP2-mediated pathways, highlighting its translational potential. However, cross-reactivity with other CRMP isoforms remains a technical consideration. Overall, CRMP2 antibodies serve as essential reagents for unraveling neural mechanisms and developing targeted therapies for neurological diseases.