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Gene Review

Camk1  -  calcium/calmodulin-dependent protein kinase I

Mus musculus

Synonyms: AI505105, CaM kinase I, CaM kinase I alpha, CaM-KI, CaMKI-alpha, ...
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Disease relevance of Camk1

  • Using a combination of pharmacological inhibitors and dominant-negative kinases (dnKinase), we identified a requirement for CaMKK acting through CaMKI in the stimulation of ERKs upon depolarization of the neuroblastoma cell line, NG108 [1].

High impact information on Camk1

  • We here searched for kinases with a core catalytic structure similar to CaMKI and CaMKIV [2].
  • Interestingly, despite a large similarity in the kinase domain, CL1/CL2/CLr had an impact on CRE-dependent gene expression distinct from that of the related CaMKI/CaMKIV and CaMKII [2].
  • ERK activation upon depolarization or transfection with constitutively active (ca) CaMKI was blocked by dnRas [1].
  • The CaMKI site, Ser(89) ((84)LLRSGSSPNL(93)), fits the expected consensus whereas the CaMKIV site, Ser(24) ((19)SSPALSASAS(28)), is novel [3].
  • The multifunctional calcium/calmodulin-dependent protein kinases I and IV (CaMKI and CaMKIV) are closely related by primary sequence and predicted to have similar substrate specificities based on peptide studies [3].

Biological context of Camk1

  • We identified a fragment of p300-(1-117) that is a substrate of both kinases, and through both mutagenesis and Edman phosphate ((32)P) release sequencing, established that CaMKI and CaMKIV phosphorylate completely different sites [3].
  • Hypertrophy-sensitive reporter activity in primary cardiomyocytes was silenced when tet-inducible CaM KII was co-expressed with plasmids harboring active forms of CaN, CaM KI or CaM KIV [4].
  • CaM-KIV as well as CaM-KI are activated upon phosphorylation by two distinct isoforms of Ca2+/calmodulin-dependent protein kinase kinases, CaM-KKs alpha and beta [5].
  • In this study, we first examined the developmental gene expression of the four isoforms of CaMKI in mouse brain with special attention to the hippocampal formation by in situ hybridization analysis [6].

Anatomical context of Camk1

  • Myocyte exposure to doxycycline (DOX) blocked tTA-driven CaM KII expression and restored CaN/CaM KI or CaN/CaM KIV driven reporter activation [4].
  • The overexpression of kinase-dead mutants of CaMKI reduced the average dendritic length of the transfected neurons without any significant effects on the number of primary dendrites and the branching index [6].

Other interactions of Camk1

  • However, there are no changes in the levels of CaMKI, which is expressed in the ventricles, or CaMKIV, which is not detectable in the ventricles [7].


  1. Calcium activation of ERK mediated by calmodulin kinase I. Schmitt, J.M., Wayman, G.A., Nozaki, N., Soderling, T.R. J. Biol. Chem. (2004) [Pubmed]
  2. Molecular identification and characterization of a family of kinases with homology to Ca2+/calmodulin-dependent protein kinases I/IV. Ohmae, S., Takemoto-Kimura, S., Okamura, M., Adachi-Morishima, A., Nonaka, M., Fuse, T., Kida, S., Tanji, M., Furuyashiki, T., Arakawa, Y., Narumiya, S., Okuno, H., Bito, H. J. Biol. Chem. (2006) [Pubmed]
  3. Proteomic analysis of calcium/calmodulin-dependent protein kinase I and IV in vitro substrates reveals distinct catalytic preferences. Corcoran, E.E., Joseph, J.D., MacDonald, J.A., Kane, C.D., Haystead, T.A., Means, A.R. J. Biol. Chem. (2003) [Pubmed]
  4. Tetracycline-inducible CaM kinase II silences hypertrophy-sensitive gene expression in rat neonate cardiomyocytes. Valencia, T.G., Roberts, L.D., Zeng, H., Grant, S.R. Biochem. Biophys. Res. Commun. (2000) [Pubmed]
  5. Distinct immunohistochemical localization of two isoforms of Ca2+/calmodulin-dependent protein kinase kinases in the adult rat brain. Sakagami, H., Umemiya, M., Saito, S., Kondo, H. Eur. J. Neurosci. (2000) [Pubmed]
  6. Spatiotemporal expression of four isoforms of Ca(2+)/calmodulin-dependent protein kinase I in brain and its possible roles in hippocampal dendritic growth. Kamata, A., Sakagami, H., Tokumitsu, H., Owada, Y., Fukunaga, K., Kondo, H. Neurosci. Res. (2007) [Pubmed]
  7. Pressure overload selectively up-regulates Ca2+/calmodulin-dependent protein kinase II in vivo. Colomer, J.M., Mao, L., Rockman, H.A., Means, A.R. Mol. Endocrinol. (2003) [Pubmed]
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