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Gene Review

Camk2d  -  calcium/calmodulin-dependent protein...

Mus musculus

Synonyms: 2810011D23Rik, 8030469K03Rik, CaM kinase II subunit delta, CaMK II, CaMK-II subunit delta, ...
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Disease relevance of Camk2d

  • Immunohistochemically, CaM kinase II alpha immunoreactivity was upregulated in the cerebral cortex and hippocampal CA1 area of scrapie-positive mice infected with ME7 scrapie strain [1].
  • Unexpectedly, beta(1)AR-induced myocyte hypertrophy and apoptosis are independent of the classic cAMP/PKA pathway, but require activation of Ca(2+)/calmodulin-dependent kinase II (CaMK II) [2].

High impact information on Camk2d

  • In RBL-2H3 m1 cells, inhibition of CaM kinase II decreased Thr-1940 phosphorylation, and inhibited release of the secretory granule marker hexosaminidase in response to carbachol but not to antigen [3].
  • Similarly, co-transfected Ala --> Thr-1940 human NMHC-IIA was phosphorylated by activated CaM kinase II in HeLa cells, while wild type was not [3].
  • Thus, although this study establishes that synapsin I is a substrate for CaM kinase II in the pancreatic beta-cell, this event appears not to be important for the mobilization of insulin granules [4].
  • A cDNA clone for the alpha subunit of mouse brain Ca2+/CaM-dependent protein kinase II (CaM-kinase II) was transcribed in vitro and translated in a rabbit reticulocyte lysate system [5].
  • These results establish that introduction of negative charge(s) at residue 286, either by autophosphorylation of Thr or by mutation to Asp, is sufficient and necessary to generate the partially Ca2+-independent form of CaM-kinase II [5].

Biological context of Camk2d

  • Proteolytic digests of these immunoprecipitates revealed that calcium primarily induced the increased phosphorylation of sites identified as CaM kinase II-specific and distinct from protein kinase A-specific sites [4].
  • The stimulation of Ca(2+)-independent (autonomous) CaMK-II enzymatic activity, a barometer of in situ activated CaMK-II, was prevented by the same KN-93 concentrations that cause G1 phase arrest [6].
  • These results suggest that D2R is involved in the activation of the nuclear isoform of CaM kinase II and thereby in stimulation of gene expression through Ca(2+) signaling [7].
  • Ca+/calmodulin-dependent protein kinase II (CaM kinase II) is regulated by calcium oscillations, autophosphorylation, and its subunit composition [8].
  • CaM kinase II is an enzyme that plays a major role in the regulation of long-term potentiation, a form of synaptic plasticity associated with learning and memory [1].

Anatomical context of Camk2d

  • To elucidate the cellular function of CaM kinase II, we introduced cDNA of wild-type CaM kinase II alpha- or beta-isoform, and of mutant alpha-isoform (Ala-286 kinase) into two different types of neuroblastoma, Neuro2a (Nb2a) and NG108-15, thus generating cell lines stably producing elevated levels of these kinases [9].
  • Some substrates of CaM kinase II related to neurite outgrowth were detected in cells overexpressing the kinase stimulated with H-7 [9].
  • Differential autophosphorylation of CaM kinase II from phasic and tonic smooth muscle tissues [8].
  • The membrane-permeable cGMP analog 8-bromo-cGMP relaxed gastric fundus smooth muscles and activated CaM kinase II [10].
  • Direct inhibition of CaMK-II in 1-day-old neurons immediately froze growth cone dynamics, disorganized F-actin and ultimately led to axon retraction [11].

Associations of Camk2d with chemical compounds

  • Serine 416, numbered according to the longest human tau isoform, has been reported to be one of the major phosphorylation sites by CaM kinase II in vitro [12].
  • SNP-induced CaM kinase II activation was prevented by KN-93 [10].
  • The soluble guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo-[4,3-alpha]quinoxalin-1-one inhibited SNP-induced relaxation and CaM kinase II activation [10].
  • Acetylcholine (ACh) increased autonomous CaM kinase II activity in fundus and proximal colon smooth muscles in a time- and dose-dependent manner [8].
  • Ryanodine, tetracaine, 2-aminoethoxydiphenylborate, and cyclopiazonic acid inhibited SNP-induced fundus smooth muscle relaxation and CaM kinase II activation [10].

Analytical, diagnostic and therapeutic context of Camk2d

  • By immunoprecipitation, in situ phosphorylation of synapsin I was induced in permeabilized betaTC3 cells within a Ca2+ concentration range shown to activate endogenous CaM kinase II under identical conditions [4].
  • When soluble CaM kinase II previously autophosphorylated was incubated with PSDs, the kinase was precipitated by centrifugation, indicating that the soluble kinase associated with PSDs and formed a PSD-CaM kinase II complex [13].
  • Immunoreactivity of CaM kinase II alpha, measured by Western blot, increased markedly in scrapie-infected brains compared with control brains [1].


  1. Increased expression of CaM kinase II alpha in the brains of scrapie-infected mice. Jin, J.K., Choi, J.K., Lee, H.G., Kim, Y.S., Carp, R.I., Choi, E.K. Neurosci. Lett. (1999) [Pubmed]
  2. Distinct beta-adrenergic receptor subtype signaling in the heart and their pathophysiological relevance. Zheng, M., Han, Q.D., Xiao, R.P. Sheng li xue bao : [Acta physiologica Sinica]. (2004) [Pubmed]
  3. Calcium-dependent threonine phosphorylation of nonmuscle myosin in stimulated RBL-2H3 mast cells. Buxton, D.B., Adelstein, R.S. J. Biol. Chem. (2000) [Pubmed]
  4. Site-specific phosphorylation of synapsin I by Ca2+/calmodulin-dependent protein kinase II in pancreatic betaTC3 cells: synapsin I is not associated with insulin secretory granules. Krueger, K.A., Ings, E.I., Brun, A.M., Landt, M., Easom, R.A. Diabetes (1999) [Pubmed]
  5. Studies of the regulatory mechanism of Ca2+/calmodulin-dependent protein kinase II. Mutation of threonine 286 to alanine and aspartate. Fong, Y.L., Taylor, W.L., Means, A.R., Soderling, T.R. J. Biol. Chem. (1989) [Pubmed]
  6. CaMK-II inhibition reduces cyclin D1 levels and enhances the association of p27kip1 with Cdk2 to cause G1 arrest in NIH 3T3 cells. Morris, T.A., DeLorenzo, R.J., Tombes, R.M. Exp. Cell Res. (1998) [Pubmed]
  7. Activation of nuclear Ca(2+)/calmodulin-dependent protein kinase II and brain-derived neurotrophic factor gene expression by stimulation of dopamine D2 receptor in transfected NG108-15 cells. Takeuchi, Y., Fukunaga, K., Miyamoto, E. J. Neurochem. (2002) [Pubmed]
  8. Differential autophosphorylation of CaM kinase II from phasic and tonic smooth muscle tissues. Lorenz, J.M., Riddervold, M.H., Beckett, E.A., Baker, S.A., Perrino, B.A. Am. J. Physiol., Cell Physiol. (2002) [Pubmed]
  9. Neurite outgrowth of neuroblastoma cells overexpressing alpha and beta isoforms of Ca2+/calmodulin-dependent protein kinase II-effects of protein kinase inhibitors. Yamauchi, T., Yoshimura, Y., Nomura, T., Fujii, M., Sugiura, H. Brain Res. Brain Res. Protoc. (1998) [Pubmed]
  10. Roles of CaM kinase II and phospholamban in SNP-induced relaxation of murine gastric fundus smooth muscles. Kim, M., Han, I.S., Koh, S.D., Perrino, B.A. Am. J. Physiol., Cell Physiol. (2006) [Pubmed]
  11. Laminin activates CaMK-II to stabilize nascent embryonic axons. Easley, C.A., Faison, M.O., Kirsch, T.L., Lee, J.A., Seward, M.E., Tombes, R.M. Brain Res. (2006) [Pubmed]
  12. Phosphorylation of tau at serine 416 by Ca2+/calmodulin-dependent protein kinase II in neuronal soma in brain. Yamamoto, H., Hiragami, Y., Murayama, M., Ishizuka, K., Kawahara, M., Takashima, A. J. Neurochem. (2005) [Pubmed]
  13. Phosphorylation-dependent reversible translocation of Ca2+/calmodulin-dependent protein kinase II to the postsynaptic densities. Yamauchi, T., Yoshimura, Y. Life Sci. (1998) [Pubmed]
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