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Camk4  -  calcium/calmodulin-dependent protein...

Mus musculus

Synonyms: A430110E23Rik, AI666733, Ca2+/calmodulin-dependent protein kinase type IV/Gr, CaM kinase-GR, CaMK IV, ...
 
 
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Disease relevance of Camk4

  • We have characterized Ca2+/calmodulin-dependent protein kinase IV (CaM kinase IV), expressed using the baculovirus/Sf9 cell system, to assess its potential role in Ca2+-dependent transcriptional regulation [1].
  • Moreover, mice null for the CaMKIV gene develop ventricular hypertrophy and induce the expression of selected hypertrophy marker mRNAs, indicating that CaMKIV is not required at any time during the development of hypertrophy [2].
  • In the absence of CaMKIV, the exchange of sperm nuclear basic proteins in male spermatids is impaired, resulting in male infertility secondary to defective spermiogenesis [3].
  • Recent studies have demonstrated that transgenic (TG) expression of either Ca2+/calmodulin-dependent protein kinase IV (CaMKIV) or CaMKIIdeltaB, both of which localize to the nucleus, induces cardiac hypertrophy [4].
 

High impact information on Camk4

 

Biological context of Camk4

 

Anatomical context of Camk4

  • Elongating spermatids are not transcriptionally active, raising the possibility that Camk4 has a novel function in male germ cells [6].
  • Multiple innervation by climbing fibers and enhanced parallel fiber synaptic currents suggested an immature development of Purkinje cells in the Camk4(-/-) mice [10].
  • Co-transfection of COS-1 cells by cDNA for CaM kinase IV gave 3-fold stimulation of a reporter gene expression, whereas co-transfection with CaM kinase II gave no transcriptional stimulation [1].
  • Consequently, T lymphocytes present in the spleen can be activated normally in response to either stimulus mentioned above, demonstrating that the effects of the inactive CaMKIV on activation are reversible [11].
  • We further demonstrate that CaMKIV expression and localization are unaffected by the absence of calspermin and that calspermin does not colocalize to the nuclear matrix with CaMKIV [12].
 

Associations of Camk4 with chemical compounds

  • The Ca(2+)/calmodulin-dependent protein kinase type IV/Gr (CaMKIV/Gr) is a key effector of neuronal Ca(2+) signaling; its function was analyzed by targeted gene disruption in mice [9].
  • On the other hand, the developmental expression of CaMKIV in brain and thymus appears to be controlled by thyroid hormone mediated via the thyroid hormone receptor alpha [13].
  • Ca2+/calmodulin-dependent protein kinase IV (CaMKIV) is a serine/threonine protein kinase with limited tissue distribution [3].
  • CONCLUSION: In view of the patterns of recombination restricted to the major dopaminoceptive regions as seen in the context of the CREB, CaMKIV and GR mutations, the D1Cre line will be a useful tool to dissect the contributions of specific genes to biological processes involving dopamine signaling [14].
  • Conversion of either serine to alanine by mutagenesis abolished CaM kinase IV inhibition of adenylyl cyclase [15].
 

Physical interactions of Camk4

 

Enzymatic interactions of Camk4

 

Co-localisations of Camk4

 

Regulatory relationships of Camk4

 

Other interactions of Camk4

  • We report here that importin alpha is able to carry CaMKIV into the nucleus without the need for importin beta or any other soluble proteins in digitonin-permeabilized cells [7].
  • However, despite impaired LTP and CREB activation, CaMKIV/Gr-deficient mice exhibited no obvious deficits in spatial learning and memory [9].
  • Short-term motor nerve stimulation (2 h at 10 Hz) likewise increased PGC-1alpha mRNA expression in tibialis anterior muscles in both Camk4(-/-) and wild-type mice [19].
  • Although the overall cytoarchitecture of the cerebellum appeared normal in the Camk4(-/-) mice, we observed a significant reduction in the number of mature Purkinje neurons and reduced expression of the protein marker calbindin D28k within individual Purkinje neurons [10].
  • 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 [2].
 

Analytical, diagnostic and therapeutic context of Camk4

References

  1. Characterization of Ca2+/calmodulin-dependent protein kinase IV. Role in transcriptional regulation. Enslen, H., Sun, P., Brickey, D., Soderling, S.H., Klamo, E., Soderling, T.R. J. Biol. Chem. (1994) [Pubmed]
  2. 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]
  3. Female fertility is reduced in mice lacking Ca2+/calmodulin-dependent protein kinase IV. Wu, J.Y., Gonzalez-Robayna, I.J., Richards, J.S., Means, A.R. Endocrinology (2000) [Pubmed]
  4. The deltaC isoform of CaMKII is activated in cardiac hypertrophy and induces dilated cardiomyopathy and heart failure. Zhang, T., Maier, L.S., Dalton, N.D., Miyamoto, S., Ross, J., Bers, D.M., Brown, J.H. Circ. Res. (2003) [Pubmed]
  5. An important role of neural activity-dependent CaMKIV signaling in the consolidation of long-term memory. Kang, H., Sun, L.D., Atkins, C.M., Soderling, T.R., Wilson, M.A., Tonegawa, S. Cell (2001) [Pubmed]
  6. Spermiogenesis and exchange of basic nuclear proteins are impaired in male germ cells lacking Camk4. Wu, J.Y., Ribar, T.J., Cummings, D.E., Burton, K.A., McKnight, G.S., Means, A.R. Nat. Genet. (2000) [Pubmed]
  7. Importin alpha transports CaMKIV to the nucleus without utilizing importin beta. Kotera, I., Sekimoto, T., Miyamoto, Y., Saiwaki, T., Nagoshi, E., Sakagami, H., Kondo, H., Yoneda, Y. EMBO J. (2005) [Pubmed]
  8. Long-Term Memory Deficits in Pavlovian Fear Conditioning in Ca2+/Calmodulin Kinase Kinase {alpha}-Deficient Mice. Blaeser, F., Sanders, M.J., Truong, N., Ko, S., Wu, L.J., Wozniak, D.F., Fanselow, M.S., Zhuo, M., Chatila, T.A. Mol. Cell. Biol. (2006) [Pubmed]
  9. Impaired synaptic plasticity and cAMP response element-binding protein activation in Ca2+/calmodulin-dependent protein kinase type IV/Gr-deficient mice. Ho, N., Liauw, J.A., Blaeser, F., Wei, F., Hanissian, S., Muglia, L.M., Wozniak, D.F., Nardi, A., Arvin, K.L., Holtzman, D.M., Linden, D.J., Zhuo, M., Muglia, L.J., Chatila, T.A. J. Neurosci. (2000) [Pubmed]
  10. Cerebellar defects in Ca2+/calmodulin kinase IV-deficient mice. Ribar, T.J., Rodriguiz, R.M., Khiroug, L., Wetsel, W.C., Augustine, G.J., Means, A.R. J. Neurosci. (2000) [Pubmed]
  11. Defective survival and activation of thymocytes in transgenic mice expressing a catalytically inactive form of Ca2+/calmodulin-dependent protein kinase IV. Anderson, K.A., Ribar, T.J., Illario, M., Means, A.R. Mol. Endocrinol. (1997) [Pubmed]
  12. Spermatogenesis and the regulation of Ca(2+)-calmodulin-dependent protein kinase IV localization are not dependent on calspermin. Wu, J.Y., Ribar, T.J., Means, A.R. Mol. Cell. Biol. (2001) [Pubmed]
  13. Regulation and properties of the rat Ca2+/calmodulin-dependent protein kinase IV gene and its protein products. Means, A.R., Ribar, T.J., Kane, C.D., Hook, S.S., Anderson, K.A. Recent Prog. Horm. Res. (1997) [Pubmed]
  14. Expression of Cre recombinase in dopaminoceptive neurons. Lemberger, T., Parlato, R., Dassesse, D., Westphal, M., Casanova, E., Turiault, M., Tronche, F., Schiffmann, S.N., Schütz, G. BMC neuroscience (2007) [Pubmed]
  15. Regulation of type I adenylyl cyclase by calmodulin kinase IV in vivo. Wayman, G.A., Wei, J., Wong, S., Storm, D.R. Mol. Cell. Biol. (1996) [Pubmed]
  16. Genetic alteration of anxiety and stress-like behavior in mice lacking CaMKIV. Shum, F.W., Ko, S.W., Lee, Y.S., Kaang, B.K., Zhuo, M. Molecular pain [electronic resource] (2005) [Pubmed]
  17. Colocalization of phosphorylated CREB with calcium/calmodulin-dependent protein kinase IV in hippocampal neurons induced by ohmfentanyl stereoisomers. Gao, C., Chen, L., Tao, Y., Chen, J., Xu, X., Zhang, G., Chi, Z. Brain Res. (2004) [Pubmed]
  18. Changes in signaling pathways regulating neuroplasticity induced by neurokinin 1 receptor knockout. Musazzi, L., Perez, J., Hunt, S.P., Racagni, G., Popoli, M. Eur. J. Neurosci. (2005) [Pubmed]
  19. Skeletal muscle adaptation in response to voluntary running in Ca2+/calmodulin-dependent protein kinase IV-deficient mice. Akimoto, T., Ribar, T.J., Williams, R.S., Yan, Z. Am. J. Physiol., Cell Physiol. (2004) [Pubmed]
  20. CaM kinase IV regulates lineage commitment and survival of erythroid progenitors in a non-cell-autonomous manner. Wayman, G.A., Walters, M.J., Kolibaba, K., Soderling, T.R., Christian, J.L. J. Cell Biol. (2000) [Pubmed]
  21. Calmodulin-dependent protein kinase IV regulates hematopoietic stem cell maintenance. Kitsos, C.M., Sankar, U., Illario, M., Colomer-Font, J.M., Duncan, A.W., Ribar, T.J., Reya, T., Means, A.R. J. Biol. Chem. (2005) [Pubmed]
  22. Chromosomal localization of the human gene for brain Ca2+/calmodulin-dependent protein kinase type IV. Sikela, J.M., Law, M.L., Kao, F.T., Hartz, J.A., Wei, Q., Hahn, W.E. Genomics (1989) [Pubmed]
  23. Ca(2+)/calmodulin-dependent protein kinase IV is expressed in spermatids and targeted to chromatin and the nuclear matrix. Wu, J.Y., Means, A.R. J. Biol. Chem. (2000) [Pubmed]
 
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