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Camk2b  -  calcium/calmodulin-dependent protein...

Mus musculus

Synonyms: CaM kinase II subunit beta, CaMK II, CaMK-II subunit beta, Calcium/calmodulin-dependent protein kinase type II subunit beta, Camk2d
 
 
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Disease relevance of Camk2b

  • The activity and levels of CaM kinase II-alpha was investigated in the cytosolic and membrane fraction of mice cerebral cortex and cerebellum using an experimental model of fatal murine cerebral malaria (FMCM) [1].
  • We reported evidence for CaM kinase II and a synapsin I-like protein present in mouse insulinoma MIN6 cells (Matsumoto, K., Fukunaga, K., Miyazaki, J., Shichiri, M., and Miyamoto, E. (1995) Endocrinology 136, 3784-3793) [2].
  • Previous studies utilizing crude brain homogenates have shown that forebrain ischemia results in inhibition of calcium/calmodulin-dependent protein kinase II (CaM kinase II) activity without large-scale proteolysis of the enzyme [3].
  • Since the expression of Ca(2+)/calmodulin-dependent protein kinase II (CaM kinase II) is regulated during brain development, the developmental change of the enzyme was investigated during the neural differentiation of murine P19 embryonal carcinoma cells [4].
  • Treating the mouse intestine with the calmodulin antagonist W-7 and KN-93, an inhibitor of Ca(2+)-calmodulin-dependent protein kinase II (CaMK II), reduced the sensitivity of the host to the action of Escherichia coli heat-stable enterotoxin II (STII) [5].
 

High impact information on Camk2b

  • To relate different forms of synaptic plasticity to the formation and maintenance of place cells in the hippocampus, we have recorded place cells in freely behaving, transgenic mice that express a mutated Ca2+-independent form of CaM Kinase II [6].
  • We have examined glutamate receptors (GluRs) as substrates for CaM-K II because (1) they are colocalized in the PSD, (2) cloned GluRs contain consensus phosphorylation sites for protein kinases including CaM-K II, and (3) several GluRs are regulated by other protein kinases [7].
  • We report here that CaM-K II phosphorylates GluR in several in vitro systems, including the PSD, and that activated CaM-K II enhances kainate-induced ion current three- to fourfold in cultured hippocampal neurons [7].
  • Regulation of GluRs, which are involved in excitatory synaptic transmission and in mechanisms of learning and memory, by CaM-K II is of interest because of the postulated role of CaM-K II in synaptic plasticity and its known involvement in induction of long-term potentiation [7].
  • In this issue of Neuron, Yasuda and Mayford report an elegant cell-type restricted inducible transgenic mouse overexpressing a mutant form of CaM kinase II selectively in superficial layers of medial entorhinal cortex and its upstream regions [8].
 

Biological context of Camk2b

  • Forty-one affected F(2) and 120 BC(1) segregants from the outcross of GP/Bc to CBA/J, and 23 affected F(2) segregants from the outcross to ICR/Bc, were used to map gp to proximal Chr 11 between the centromere and D11Dal1 (Camk2b), an interval previously defined as less than 1 cM [9].
  • These correlative observations caused us to test whether activation of CaM kinase II mediated the chromosomal transit into an anaphase configuration [10].
  • CaM kinase II-alpha activity, levels and Ca/calmodulin dependent phosphorylation of substrate proteins in mice brain during fatal murine cerebral malaria [1].
  • CaM kinase II constitutes a family of multifunctional protein kinases that play a major role in Ca2+-mediated signal transduction [11].
  • The beta-subunit of calmodulin kinase II (beta-CaMK II) is a good candidate for the wr mutation because of its chromosomal localization and tissue distribution [12].
 

Anatomical context of Camk2b

  • CaM kinase II appears localized on midzone microtubules as soon as they form and may have a role in specifying the position of the contractile ring of the second polar body [10].
  • These data suggest that CaM kinase II dephosphorylation and deactivation in the pancreatic beta-cell is mediated by the combined action of an okadaic-acid-sensitive phosphatase and a Mg2+-dependent phosphatase, such as PP-2C [13].
  • These data show for the first time that Ca/CaMK II activation plays an important role in the transmission of GnRH signals from the plasma membrane to the LH subunit genes [14].
  • Additionally, we describe the murine betaM-CaM kinase II, a variant of the 'brain-specific' beta-CaM kinase II, which is highly expressed in skeletal muscle [11].
  • Pathology of FMCM resulted in decreased CaM kinase-II activity in both cortex and cerebellum though western analysis revealed no appreciable changes in the levels of CaM kinase-II alpha in cytosol and membrane fractions from control and cerebral malaria infected brain [1].
 

Associations of Camk2b with chemical compounds

  • Blocking calcium influx with nimodipine or depleting intracellular calcium storage pools with thapsigargin each resulted in a partial suppression of GnRH-induced activation of Ca/CaMK II, and in combination, completely suppressed the Ca/CaMK II response to GnRH [14].
  • The calcium channel activator Bay K 8644 stimulated a 3-fold increase in Ca/CaMK II activity, similar to GnRH [14].
  • Under these conditions, CaM kinase II phosphatase was more sensitive to calyculin A relative to okadaic acid, characteristic of the involvement of PP-1 [13].
  • CaM kinase II phosphorylation of slo Thr107 regulates activity and ethanol responses of BK channels [15].
  • Quantitative determination of CaMK II isoform mRNA was carried out in several tissues and beta cells purified by fluorescence activated cell sorting and compared to the housekeeping enzyme pyruvate dehydrogenase [16].
 

Enzymatic interactions of Camk2b

 

Regulatory relationships of Camk2b

 

Other interactions of Camk2b

 

Analytical, diagnostic and therapeutic context of Camk2b

References

  1. CaM kinase II-alpha activity, levels and Ca/calmodulin dependent phosphorylation of substrate proteins in mice brain during fatal murine cerebral malaria. Kumar, K.A., Babu, P.P. Neurosci. Lett. (2003) [Pubmed]
  2. Cloning from insulinoma cells of synapsin I associated with insulin secretory granules. Matsumoto, K., Ebihara, K., Yamamoto, H., Tabuchi, H., Fukunaga, K., Yasunami, M., Ohkubo, H., Shichiri, M., Miyamoto, E. J. Biol. Chem. (1999) [Pubmed]
  3. Global forebrain ischemia results in decreased immunoreactivity of calcium/calmodulin-dependent protein kinase II. Churn, S.B., Yaghmai, A., Povlishock, J., Rafiq, A., DeLorenzo, R.J. J. Cereb. Blood Flow Metab. (1992) [Pubmed]
  4. Induction and alternative splicing of delta isoform of Ca(2+)/calmodulin-dependent protein kinase II during neural differentiation of P19 embryonal carcinoma cells and during brain development. Donai, H., Murakami, T., Amano, T., Sogawa, Y., Yamauchi, T. Brain Res. Mol. Brain Res. (2000) [Pubmed]
  5. Involvement of Ca(2+)-calmodulin-dependent protein kinase II in the intestinal secretory action of Escherichia coli heat-stable enterotoxin II. Fujii, Y., Nomura, T., Yamanaka, H., Okamoto, K. Microbiol. Immunol. (1997) [Pubmed]
  6. Mice expressing activated CaMKII lack low frequency LTP and do not form stable place cells in the CA1 region of the hippocampus. Rotenberg, A., Mayford, M., Hawkins, R.D., Kandel, E.R., Muller, R.U. Cell (1996) [Pubmed]
  7. Phosphorylation and regulation of glutamate receptors by calcium/calmodulin-dependent protein kinase II. McGlade-McCulloh, E., Yamamoto, H., Tan, S.E., Brickey, D.A., Soderling, T.R. Nature (1993) [Pubmed]
  8. Inducible and cell-type restricted manipulation in the entorhinal cortex. Nakazawa, K. Neuron (2006) [Pubmed]
  9. Gaping lids, gp, a mutation on centromeric chromosome 11 that causes defective eyelid development in mice. Juriloff, D.M., Harris, M.J., Banks, K.G., Mah, D.G. Mamm. Genome (2000) [Pubmed]
  10. Calcium/calmodulin-dependent protein kinase II and calmodulin: regulators of the meiotic spindle in mouse eggs. Johnson, J., Bierle, B.M., Gallicano, G.I., Capco, D.G. Dev. Biol. (1998) [Pubmed]
  11. Developmental expression of the CaM kinase II isoforms: ubiquitous gamma- and delta-CaM kinase II are the early isoforms and most abundant in the developing nervous system. Bayer, K.U., Löhler, J., Schulman, H., Harbers, K. Brain Res. Mol. Brain Res. (1999) [Pubmed]
  12. Exclusion of the beta-subunit of type II calmodulin kinase for the wobbler spinal muscular atrophy gene. Bronstein, J.M., Yamashita, C., Farber, D.B. Brain Res. Mol. Brain Res. (1996) [Pubmed]
  13. Dephosphorylation and deactivation of Ca2+/calmodulin-dependent protein kinase II in betaTC3-cells is mediated by Mg2+- and okadaic-acid-sensitive protein phosphatases. Easom, R.A., Tarpley, J.L., Filler, N.R., Bhatt, H. Biochem. J. (1998) [Pubmed]
  14. The calcium component of gonadotropin-releasing hormone-stimulated luteinizing hormone subunit gene transcription is mediated by calcium/calmodulin-dependent protein kinase type II. Haisenleder, D.J., Ferris, H.A., Shupnik, M.A. Endocrinology (2003) [Pubmed]
  15. CaM kinase II phosphorylation of slo Thr107 regulates activity and ethanol responses of BK channels. Liu, J., Asuncion-Chin, M., Liu, P., Dopico, A.M. Nat. Neurosci. (2006) [Pubmed]
  16. Cloning and quantitative determination of the human Ca2+/calmodulin-dependent protein kinase II (CaMK II) isoforms in human beta cells. Rochlitz, H., Voigt, A., Lankat-Buttgereit, B., Göke, B., Heimberg, H., Nauck, M.A., Schiemann, U., Schatz, H., Pfeiffer, A.F. Diabetologia (2000) [Pubmed]
  17. alphaKAP is an anchoring protein for a novel CaM kinase II isoform in skeletal muscle. Bayer, K.U., Harbers, K., Schulman, H. EMBO J. (1998) [Pubmed]
  18. Ca2+/calmodulin-dependent protein kinase II and synapsin I-like protein in mouse insulinoma MIN6 cells. Matsumoto, K., Fukunaga, K., Miyazaki, J., Shichiri, M., Miyamoto, E. Endocrinology (1995) [Pubmed]
  19. Role of beta isoform-specific insertions of Ca2+/calmodulin-dependent protein kinase II. Urushihara, M., Yamauchi, T. Eur. J. Biochem. (2001) [Pubmed]
  20. CaM kinase II and phospholamban contribute to caffeine-induced relaxation of murine gastric fundus smooth muscle. Kim, M., Cho, S.Y., Han, I.S., Koh, S.D., Perrino, B.A. Am. J. Physiol., Cell Physiol. (2005) [Pubmed]
  21. Phosphorylation and inhibition of olfactory adenylyl cyclase by CaM kinase II in Neurons: a mechanism for attenuation of olfactory signals. Wei, J., Zhao, A.Z., Chan, G.C., Baker, L.P., Impey, S., Beavo, J.A., Storm, D.R. Neuron (1998) [Pubmed]
  22. Overexpression of Ca2+/calmodulin-dependent protein kinase II in Neuro2a and NG108-15 neuroblastoma cell lines promotes neurite outgrowth and growth cone motility. Goshima, Y., Ohsako, S., Yamauchi, T. J. Neurosci. (1993) [Pubmed]
  23. Overexpression of Ca2+/calmodulin-dependent protein kinase II inhibits neurite outgrowth of PC12 cells. Tashima, K., Yamamoto, H., Setoyama, C., Ono, T., Miyamoto, E. J. Neurochem. (1996) [Pubmed]
  24. Regional differences between the immunohistochemical distribution of Ca2+/calmodulin-dependent protein kinase II alpha and beta isoforms in the brainstem of the rat. Ochiishi, T., Yamauchi, T., Terashima, T. Brain Res. (1998) [Pubmed]
 
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