Product Pathways - Neuroscience
CaMKII-α (D10C11) Rabbit mAb #11945
|W||H M R||Endogenous||50||Rabbit IgG|
Reactivity Key: H=Human M=Mouse R=Rat
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Specificity / Sensitivity
CaMKII-α (D10C11) Rabbit mAb recognizes endogenous levels of total CaMKII-α protein. The peptide sequence used as the antigen is not conserved in CaMKII-β, -γ, and -δ.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human CaMKII-α protein.
Western blot analysis of extracts from 293T cells, mock transfected (-) or transfected with a construct expressing Myc-tagged full-length human CaMKII-α (hCaMKII-α-Myc;+), CaMKII-β (hCaMKII-β-Myc;+), or CaMKII-δ (hCaMKII-δ-Myc;+), and mouse brain using CaMKII-α (D10C11) Rabbit mAb (upper) or Myc-Tag (71D10) Rabbit mAb #2278 (lower).
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).
- Hughes, K. et al. (2001) J. Biol. Chem. 276, 36008-36013.
- Barria, A. et al. (1997) Science 276, 2042-2045.
- Barkai, U. et al. (2000) Mol. Endocrinol. 14, 554-563.
- Makhinson, M. et al. (1999) J. Neurosci. 19, 2500-2510.
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For Research Use Only. Not For Use In Diagnostic Procedures.