Our CRMP2 (Thr-555) rabbit polyclonal phosphospecific primary antibody from PhosphoSolutions is produced in-house. It detects human, mouse, and rat CRMP2 (Thr-555) and is antigen affinity purified. It is great for use in WB, ICC.
Western blot of rat PC12 cells untreated (lanes 1 & 3) or treated with calyculin A (lanes 2 & 4). The blot was probed with anti-CRMP2 (C-terminal Region) antibody (lanes 1 & 2) or anti-CRMP2 (Thr-555) antibody (lanes 3 & 4).
CRMP2 (CRMP-62, TOAD-64, DRP-2) is a microtubule associated protein involved in neuron development and axon pathfinding. CRMP2 binds to tubulin heterodimers and promotes microtubule assembly. The overexpression of CRMP2 facilitates the rate of axonal growth, whereas the mutated form that lacks activity toward the microtubule assembly inhibits axonal growth in a dominant negative manner. Phosphorylation of CRMP2 regulates its activity and this type of regulation has been implicated in axon growth cone collapse induced by several repulsive cues. Cdk5 and GSK3 phosphorylation occurs downstream of the repulsive cue, Sema-3A. Several residues in CRMP2 are phosphorylated by GSK3 (Ser-518,Thr-514, and Thr-509), and a priming site (Ser-522). These sites are conserved in human CRMP1 and CRMP4, but not in CRMP3 or CRMP5. The priming site is also phosphorylated by Cdk5. In contrast, ROCK phosphorylates Thr-555 leading to LPA, MAG, or Ephrin-A5 mediated growth cone collapse. Thus, CRMP2 phosphorylation status may be a critical element of pathways that control axon pathfinding.
Antigen Affinity Purified
Polyclonal
IgG
ICC, WB
Rabbit
DPYSL2
70
Phospho-CRMP2 (Thr-555) synthetic peptide (coupled to carrier protein) corresponding to amino acids surrounding Thr-555 in human CRMP2. This sequence is conserved in rat and mouse CRMP2 and the phospho-site is not conserved in other CRMP family members.
Human, Mouse, Rat
Storage at -20°C is recommended, as aliquots may be taken without freeze/thawing due to presence of 50% glycerol. Stable for at least 1 year at -20°C.
Liquid
PBS + 1 mg/ml BSA, 0.05% NaN3 and 50% glycerol
WB: 1:1000
ICC: 1:200
Unconjugated
This antibody was cross-adsorbed to unphosphorylated CRMP2 (Thr-555) before affinity purification using phospho-CRMP2 (Thr-555) peptide (without carrier). The antibody detects a 70 kDa* protein corresponding to CRMP2 on immunoblots of rat PC12 or mouse C2C12 cells treated with calyculin A. This reactivity can be specifically blocked using phospho-CRMP2 (Thr-555) peptide (CX2255).
Phosphorylated
Thr-555
Western blots performed on each lot.
For research use only. Not intended for therapeutic or diagnostic use. Use of all products is subject to our terms and conditions, which can be viewed on our website.
United States
After date of receipt, stable for at least 1 year at -20°C.
Salvador, V.R., et al. 2016. Anti-glycan antibodies halt axon regeneration in a model of Guillain Barrè Syndrome axonal neuropathy by inducing microtubule disorganization via RhoA-ROCK-dependent inactivation of CRMP-2. Experimental Neurology, 42-53.
Sutinen, E.M., et al. 2014. Interleukin-18 alters protein expressions of neurodegenerative diseases-linked proteins in human SH-SY5Y neuron-like cells. Frontiers in Cellular Neuroscience, 214.
Yoneda, A., et al. 2012. A collapsin response mediator protein 2 isoform controls myosin II-mediated cell migration and matrix assembly by trapping ROCK II. Molecular and Cellular Biology, 1788-1804.
Crews, L., et al. 2011. Phosphorylation of collapsin response mediator protein-2 disrupts neuronal maturation in a model of adult neurogenesis: Implications for neurodegenerative disorders. Molecular Neurodegeneration, 67.
Quarta, S, et al. 2017. Sphingosine-1-Phosphate and the S1P3 Receptor Initiate Neuronal Retraction via RhoA/ROCK Associated with CRMP2 Phosphorylation. Frontiers in molecular neuroscience, 317.
Crews, L., et al. 2011. Phosphorylation of collapsin response mediator protein-2 disrupts neuronal maturation in a model of adult neurogenesis: Implications for neurodegenerative disorders. Molecular Neurodegeneration, 67.
Moutal, A, et al. 2019. Cdk5-mediated CRMP2 phosphorylation is necessary and sufficient for peripheral neuropathic pain. Neurobiology of pain (Cambridge, Mass.), 100022.
Salvador, V.R., et al. 2016. Anti-glycan antibodies halt axon regeneration in a model of Guillain Barrè Syndrome axonal neuropathy by inducing microtubule disorganization via RhoA-ROCK-dependent inactivation of CRMP-2. Experimental Neurology, 42-53.
Yoneda, A., et al. 2012. A collapsin response mediator protein 2 isoform controls myosin II-mediated cell migration and matrix assembly by trapping ROCK II. Molecular and Cellular Biology, 1788-1804.
Crews, L., et al. 2011. Phosphorylation of collapsin response mediator protein-2 disrupts neuronal maturation in a model of adult neurogenesis: Implications for neurodegenerative disorders. Molecular Neurodegeneration, 67.
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