Cell Signaling Technology

Product Pathways - Neuroscience

Phospho-CaMKII (Tyr231) Antibody #3356

Applications Reactivity Sensitivity MW (kDa) Source
W R (H) Endogenous 50 Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  R=Rat
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

Phospho-CaMKII (Tyr231) Antibody detects endogenous levels of CaMKII only when phosphorylated at Tyr231.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Tyr231 of human CaMKII. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from rat brain, either sham-operated, 15 min ischemia followed by 4 h reperfusion or 15 min ischemia only, using Phospho-CaMKII (Tyr231) Antibody (upper) or CaMKII Antibody (lower).

Background

CaMKII is an important member of the calcium/calmodulin-activated protein kinase family, functioning in neural synaptic stimulation and T cell receptor signaling (1,2). CaMKII has catalytic and regulatory domains. Ca2+/calmodulin binding to the CaMKII regulatory domain relieves autoinhibition and activates the kinase (3). The activated CaMKII further autophosphorylates at Thr286 to render the kinase constitutively active (3). The threonine phosphorylation state of CaMKII can be regulated through PP1/PKA. PP1 (protein phosphatase 1) dephosphorylates phospho-CaMKII at Thr286. PKA (protein kinase A) prevents phospho-CaMKII (Thr286) dephosphorylation through an inhibitory effect on PP1 (4).

Phospho-CaMKII (Tyr231) Antibody is directed against a previously unpublished CaMKII tyrosine phosphorylation site at Tyr231 that was identified at Cell Signaling Technology (CST) using PhosphoScan®, CST's MS/MS platform for phosphorylation site discovery. Phosphorylation of CamKII at Tyr231 was observed in extracts isolated from ischemic rat brain.

  1. Hughes, K. et al. (2001) J. Biol. Chem. 276, 36008-36013.
  2. Barria, A. et al. (1997) Science 276, 2042-2045.
  3. Barkai, U. et al. (2000) Mol. Endocrinol. 14, 554-563.
  4. Makhinson, M. et al. (1999) J. Neurosci. 19, 2500-2510.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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