Calmodulin kinase

Protein phosphorylation Calmodulin kinase I ATI Elongation factor-2 kinase Phosphorylase kinase Myosin Light Chain kinase... 

Other mechanisms have also been implicated in odor adaptation, including cAMP-dependent phosphorylation of ciliary proteins via protein kinase A G-protein-receptor kinase activity (GRK3), possibly via phosphorylation of the OR Ca2+/calmodulin kinase II (CaMKII) phosphorylation of ACIII cGMP and carbon monoxide [ 31 ]. These latter three mechanisms have been particularly linked to longer-lasting forms of adaptation, on the order of tens of seconds (for CaMKII) or minutes (CO/cGMP). Together with the short-term adaptation described above, these various molecular mechanisms provide the OSN with a number of ways to fine-tune odor responses over time. 

Upon binding calcium ions, the small acidic protein known as calmodulin can activate enzymes by binding to a wide variety of proteins containing cahnodulin-binding domains. Such proteins include cAMP phosphodiesterase, calmodulin-dependent nitric oxide synthase, calmodulin kinases, the plasma membrane calcium pump, calcineurin, and calmodulin-dependent inositol-(l,4,5)-trisphosphate 3-kinase. See also Activation Autoinhibition... 

AC VIII, adenylyl cyclase type VIII BDNF, brain-derived neurotrophic factor CamKII, calcium-calmodulin kinase II GIRK2, G protein-activated inward rectifying potassium 2 MAOA, monoamine oxidase A n.d., not determined NCAM, neural cell adhesion molecule nNOS, neuronal nitric oxide synthase Petl, ETS domain transcription factor tPA, serine protease tissue-plasminogen activator (tPA). t/ > Increase/decrease in anxiety-related behavior. No effect. 

Cheetham SC, Crompton MR, Katona CL, Horton RW (1990) Brain 5-HTl binding sites in depressed suicides. Psychopharmacology (Berl) 102 544-548 Chen C, Rainnie DC, Greene RW, Tonegawa S (1994) Abnormal fear response and aggressive behavior in mutant mice deficient for alpha-calcium-calmodulin kinase II. Science 266 291-294... 

Furthermore, the LPS signal transduction involves the activation of G proteins, of phospholipases C and D, the formation of diacyl-glycerol (DG) and inositol triphosphate (IP3). DG mediates the stimulation of protein kinase C (PKC) and IP3 induces an increase of cytosolic Ca++ The LPS signaling pathway also involves tyrosine kinases, constitutive nitric oxide (NO) synthase (cNOS), cGMP-dependent protein kinase, Ca channels, calmodulin and calmodulin kinase [27,28], as well as the MAP kinases [29] ERK1, ERK2 and p38 [23], The intracellular events in response to LPS are due to lipid A because they are inhibited by polymyxin B which is known to bind lipid A [27] and they are reproduced by lipids A [30,31]. 

CaM kinase II <1, 3> ( phosphorylates and activates [26] <3> phosphorylation of Thr-311 results in 8-lOfold enzyme activation in the presence of 0.01 mM free Ca " and 0.002 mM calmodulin and in a 25fold increase in sensitivity to the Ca /calmodulin complex [26] <1,3> phosphorylation of isoenzyme B by calmodulin kinase II and protein kinase C added together results in a maximal 60-70fold activation, no effect on the sensitivity to the Ca2 /calmodulin complex, CaM kinase II alone activates 35-40fold in the presence of Ca " and calmodulin [28] <1> endogenous activator of isoform A [30]) [26, 28, 30]... 

Glutamate-mediated Ca2+ entry through NMDA at the plasma membrane level and mobilization of Ca2+from intracellular stores through PLC-mediated generation of PtdIns-3/J is indispensable for the basal NF-kB activity. Three cytosolic Ca2+ sensors, calmodulin, protein kinases C (PKC), and the p2 l(ras)/phosphatidylinositol 3-kinase (Ptdlns-3K)/Akt pathways, are simultaneously involved in the steps linking the Ca2+ to NF-kB activity (Lilienbaum and Israel, 2003 Marchetti et al., 2004 Lubin et al., 2005). Calmodulin modulates calcineurin, a Ca2+-dependent protein phosphatase, which plays a role in the basal NF-kB activity, whilst stimulation of both the calmodulin kinase II and Akt kinase pathways results in the up-regulation of the transcriptional potential of the p65 subunit of NF-/cB (Lilienbaum and Israel,... 

Mizuno, K., Ris, L., Sanchez-Capelo, A., Godaux, E. and Giese, K. P., 2006, Ca2+/Calmodulin Kinase Kinase alpha Is Dispensable for Brain Development But Is Required for Distinct Memories in Male, Though Not in Female, Mice, Mol Cell Biol, pp in press. 

Naito, Y., Watanabe, Y., Yokokura, H., Sugita, R., Nishio, M. and Hidaka, H., 1997, Isoform-specific activation and structural diversity of calmodulin kinase I, J Biol Chem, 272, pp 32704-8. 

Rasmussen, C. D., 2000, Cloning of a calmodulin kinase I homologue from Schizosaccharomyces pombe, J Biol Chem, 275, pp 685-90. 

Schmitt, J. M., Guire, E. S., Saneyoshi, T. and Soderling, T. R., 2005, Calmodulin-dependent kinase kinase/calmodulin kinase I activity gates extracellular-regulated kinase-dependent long-term potentiation, J Neurosci, 25, pp 1281-90. 

Sun, Z., Sassone-Corsi, P. and Means, A. R., 1995, Calspermin gene transcription is regulated by two cyclic AMP response elements contained in an alternative promoter in the calmodulin kinase TV gene, Molecular and Cellular Biology, 15, pp 561—571. 

Tokumitsu, H. and Soderling, T. R., 1996, Requirements for calcium and calmodulin in the calmodulin kinase activation cascade, J Biol Chem, 271, pp 5617-22. 

Wu, G. Y., Deisseroth, K. and Tsien, R. W., 2001, Activity-dependent CREB phosphorylation convergence of a fast, sensitive calmodulin kinase pathway and a slow, less sensitive mitogen-activated protein kinase pathway, Proc Natl Acad Sci USA, 98, pp 2808—13. 

Fog JU, Khoshbouei H, Holy M, Owens WA, Vaegter CB, Sen N, Nikandrova Y, Bowton E, McMahon DG, Colbran RJ, Daws LC, Sitte HH, Javitch JA, Galli A, Gether U (2006) Calmodulin kinase II interacts with the dopamine transporter C terminus to regulate amphetamine-induced reverse transport. Neuron 51 417—429. 

Meshul CK, Tan SE (1994) Haloperidol-induced morphological alterations are associated with changes in calcium/calmodulin kinase II activity and glutamate immunoreactivity. Synapse 75 205-217... 

An important predictor of arrhythmia is changes in the duration of the QT trace, the time for ventricular repolarization, displacement of the ST-segment, and changes in the pattern of T-waves that may sometimes be seen as a T and U wave (Roden, 2004, 2008). It can be linked to ventricular tachycardia, including TdP. Lengthened QT increases the time available for intracellular calcium accumulation, enabling early after-depolarization (BAD) in the Purkinje fibers, and activates calmodulin (CaM) and calmodulin kinase (CaMK). CaMK is believed to enhance after-... 

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