Product: Phospho-CRMP2 (Thr514) Antibody
Catalog: AF3459
Description: Rabbit polyclonal antibody to Phospho-CRMP2 (Thr514)
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
Mol.Wt.: 65/70kDa; 62kD(Calculated).
Uniprot: Q16555
RRID: AB_2834897

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 100ul $280 In stock
 200ul $350 In stock

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Product Info

WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Pig(100%), Bovine(100%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%), Chicken(100%), Xenopus(86%)
Phospho-CRMP2 (Thr514) Antibody detects endogenous levels of CRMP2 only when phosphorylated at Threonine 514.
Cite Format: Affinity Biosciences Cat# AF3459, RRID:AB_2834897.
The antibody is from purified rabbit serum by affinity purification via sequential chromatography on phospho-peptide and non-phospho-peptide affinity columns.
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.


Collapsin response mediator protein 2; Collapsin response mediator protein; Collapsin response mediator protein hCRMP 2; CRAM; CRMP 2; CRMP-2; CRMP2; DHPRP 2; DHPRP2; Dihydropyrimidinase 2; Dihydropyrimidinase like 2; Dihydropyrimidinase like 2 long form; Dihydropyrimidinase related protein 2; Dihydropyrimidinase-related protein 2; DPYL 2; DPYL2; DPYL2_HUMAN; DPYSL 2; Dpysl2; DRP-2; DRP2; Musunc 33; Musunc33; N2A3; TOAD 64; TOAD64; ULIP 2 protein; ULIP-2; Ulip2; Unc-33-like phosphoprotein 2;




CRMP-2 is an enzyme with dihydropyrimidinase activity. Plays a role in RhoA-dependent signaling, through interaction with and regulation of Rho kinase. Plays a role in neurogenesis. Aberrantly expressed in fetal Down syndrome brain.



Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - Q16555 As Substrate

Site PTM Type Enzyme
S2 Phosphorylation
T13 Phosphorylation
S14 Phosphorylation
S30 Phosphorylation
Y32 Phosphorylation P06241 (FYN)
T57 Phosphorylation
T74 Phosphorylation
S85 Phosphorylation
K254 Ubiquitination
K258 Ubiquitination
K270 Ubiquitination
T280 Phosphorylation
K293 Ubiquitination
S304 Phosphorylation
S308 Phosphorylation
K345 Acetylation
K345 Ubiquitination
T358 Phosphorylation
K368 Ubiquitination
K374 Ubiquitination
K390 Ubiquitination
S416 Phosphorylation
K418 Ubiquitination
K423 Ubiquitination
T424 Phosphorylation
Y431 Phosphorylation
C439 S-Nitrosylation
K472 Ubiquitination
Y479 Phosphorylation P07947 (YES1)
R492 Methylation
Y499 Phosphorylation
C504 S-Nitrosylation
S507 Phosphorylation
T509 Phosphorylation P49841 (GSK3B)
K511 Ubiquitination
T512 Phosphorylation
T514 Phosphorylation P49841 (GSK3B)
S517 Phosphorylation
S518 Phosphorylation P49840 (GSK3A) , P49841 (GSK3B)
K520 Acetylation
K520 Ubiquitination
T521 Phosphorylation
S522 Phosphorylation Q92630 (DYRK2) , Q00535 (CDK5)
K525 Acetylation
K525 Ubiquitination
S537 Phosphorylation
S540 Phosphorylation
S542 Phosphorylation
T554 Phosphorylation
T555 Phosphorylation Q13464 (ROCK1) , O75116 (ROCK2)
R565 Methylation
T569 Phosphorylation
S570 Phosphorylation

Research Backgrounds


Plays a role in neuronal development and polarity, as well as in axon growth and guidance, neuronal growth cone collapse and cell migration. Necessary for signaling by class 3 semaphorins and subsequent remodeling of the cytoskeleton. May play a role in endocytosis.


3F4, a monoclonal antibody which strongly stains neurofibrillary tangles in Alzheimer disease brains, specifically labels DPYSL2 when phosphorylated on Ser-518, Ser-522 and Thr-509.

Phosphorylation at Thr-514 by GSK3B abolishes tubulin-binding leading to destabilization of microtubule assembly in axons and neurodegeneration (By similarity). Phosphorylation by DYRK2 at Ser-522 is required for subsequent phosphorylation by GSK3B.

Subcellular Location:

Cytoplasm>Cytosol. Cytoplasm>Cytoskeleton. Membrane.
Note: Tightly but non-covalently associated with membranes.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:


Subunit Structure:

Homotetramer, and heterotetramer with CRMP1, DPYSL3, DPYSL4 or DPYSL5. Interacts through its C-terminus with the C-terminus of CYFIP1/SRA1. Interacts with HTR4. Interacts with CLN6. Interacts with MICALL1.


Belongs to the metallo-dependent hydrolases superfamily. Hydantoinase/dihydropyrimidinase family.

Research Fields

· Organismal Systems > Development > Axon guidance.   (View pathway)


1). Neuropilin-2 Signaling Modulates Mossy Fiber Sprouting by Regulating Axon Collateral Formation Through CRMP2 in a Rat Model of Epilepsy. MOLECULAR NEUROBIOLOGY (PubMed: 36044155) [IF=5.1]

Application: WB    Species: Rat    Sample: hippocampal

Fig. 6Sema3F/Npn-2 signaling regulates CRMP2 phosphorylation. A Reduction of CRMP2 phosphorylation in Npn-2 knockdown tissues. Adult rat hippocampi injected with various viruses as indicated were subjected to western blot with different phospho-CRMP2 antibodies. The levels of p-S522, p-T514, and p-T555-CRMP2 were significantly reduced in Npn-2 knockdown animals compared with the control group while the expression of CRMP2 was not changed, and the knockdown effects were rescued by the expression of hNpn-2. B–E Quantitation of A. n = 4, *P < 0.05, ***P < 0.001. F Semaphorin induced CRMP2 phosphorylation in primary cultures. Primary cultured neurons were treated with 5 nM AP, AP-Sema3F, or AP-Sema3A for 12 h. CRMP2 phosphorylation levels were detected by various phospho-CRMP2 antibodies as indicated using western blot. Sema3F treatment upregulated the levels of p-S522, p-T514, and p-T555-CRMP2 while made no effect on CRMP2 expression. G–J Quantitation of F. n = 4, *P < 0.05, **P < 0.01. One-way ANOVA, post hoc Tukey test. Error bars represent SEM. K Time course of Sema3F regulating CRMP2 phosphorylation. Primary cultured neurons were treated with 5 nM AP-Sema3F for 5 min, 30 min, 60 min, 6 h, 12 h, and 24 h. Levels of CRMP2 phosphorylation were detected by various phospho-CRMP2 antibodies as indicated using western blot. The levels of p-S522-CRMP2, p-T514-CRMP2, and p-T555-CRMP2 increased over time and peaked at around 12 h, while CRMP2 expression was not significantly changed. L Quantitation of K (n = 3). M Sema3F that regulates CRMP2 phosphorylation is dose-dependent. Primary cultured neurons were treated with AP-Sema3F at various doses as indicated for 12 h. CRMP2 phosphorylation levels were detected by phospho-CRMP2 antibodies as indicated using western blot. The levels of p-S522-CRMP2, p-T514-CRMP2, and p-T555-CRMP2 were increased over increased doses and peaked around 0.5 nM, while the expression of CRMP2 was not significantly changed. N Quantitation of M (n = 3)

2). aFGF Promotes Neurite Growth by Regulating GSK3β-CRMP2 Signaling Pathway in Cortical Neurons Damaged by Amyloid-β. JOURNAL OF ALZHEIMERS DISEASE (PubMed: 31561361) [IF=4.0]

Application: WB    Species: mouse    Sample: N2a-APP cells

Fig. 5. | The interaction between GSK3 and CRMP2 was validated. A) CRMP2 was detectable by immunoblotting coupled with co-IP.Representative immunoblots (B) and quantification expression of GSK3, CRMP2, and their phosphorylation levels in N2a-APP cells treated with aFGF for 24 h (C-F).

3). CRMP2 modulates mossy fiber sprouting in dentate gyrus of pilocarpine induced rat model of epilepsy. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS (PubMed: 35334412) [IF=3.1]

4). Calycosin-7-O-β-D-Glucoside Treatment Promotes Axonal Regeneration via Rho/ROCK Pathway After Ischemia/Reperfusion Injury. Research Square

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