Cell Signaling Technology

Product Pathways - Neuroscience

CaMKI-δ Antibody #3365

Applications Reactivity Sensitivity MW (kDa) Source
W H R (M) Endogenous 43 Rabbit

Applications Key:  W=Western Blotting
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.

Protocols

Specificity / Sensitivity

CaMKI-δ Antibody detects endogenous levels of total CamKI-δ protein. This antibody may detect other isoforms of CaMKI.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to human CaMKI-δ. Antibodies are purified by peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from HeLa cells, transfected with a construct overexpressing CaMKI-δ, and rat skeletal muscle using CaMKI-δ Antibody.

Background

The Ca2+/calmodulin-dependent kinase (CaMK) family, which is activated in response to elevation of intracellular Ca2+, includes CaMKI, CaMKII, CaMKIV and CaMK-kinases (CaMKKs) (1,2). CaMKI is a downstream substrate of CaMKK and has 4 isoforms: CaMKI-α, CaMKI-β, CaMKI-γ and CaMKI-δ. CaMKI is present in most cell types and may be involved in cellular functions including transcription, cytoskeletal organization, axonal growth cone motility and long-term potentiation in neurons (3-6). CaMKII is also ubiquitously expressed in most cell types. While muscular CaMKII has been linked to activation of mitochondrial biogenesis in muscle hypertrophy response, neuronal CaMKII regulates important neuronal functions, including neurotransmitter synthesis, neurotransmitter release, modulation of ion channel activity, cellular transport, cell morphology and neurite extension, synaptic plasticity, learning and memory and gene expression (7). Like CaMKI, CaMKIV is also a substrate of CaMKKs and is primarily restricted to the nucleus of neurons. CaMKIV regulates gene transcription in neurons through phosphorylation of transcription factors such as CREB and is required for fear memory (8).

Ca<KI-δ translocates to the nucleus upon intracellular Ca2+ influx and is activated through phosphorylation of Thr180 by CaMKK (9).

  1. Chin, E.R. (2004) Proc. Nutr. Soc. 63, 279-286.
  2. Mizuno, K. and Giese, K.P. (2005) J. Pharmacol. Sci. 98, 191-197.
  3. Wayman, G.A. et al. (2004) J. Neurosci. 24, 3786-3794.
  4. Gardner, H.P. et al. (2000) Genomics 63, 279-288.
  5. Verploegen, S. et al. (2005) Blood 106, 1076-1083.
  6. Takemoto-Kimura, S. et al. (2003) J. Biol. Chem. 278, 18597-18605.
  7. Yamauchi, T. (2005) Biol. Pharm. Bull. 28, 1342-1354.
  8. Wei, F. et al. (2002) Nat. Neurosci. 5, 573-579.
  9. Sakagami, H. et al. (2005) Eur. J. Neurosci. 22, 2697-2707.

Application References

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

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