Disease relevance of Chka

• Thus, the MHC and CK genes respond differently to either cardiac hypertrophy or a reduction in thyroid hormone levels [1].
• Myristoylated alanine-rich C-kinase substrate is phosphorylated and translocated by a phorbol ester-insensitive and calcium-independent protein kinase C isoform in C6 glioma cell membranes [2].
• The receptor for activated C kinase (RACK1) mRNA expression in kidneys obtained from rats 12 h following ischemia is enhanced twofold compared with sham-operated rats [3].

High impact information on Chka

• Under these conditions, Cx selectively prevented the degradation of CK mRNA in a reversible manner [4].
• Addition of insulin accompanying the withdrawal of the mitogenic stimulus of serum to myoblasts caused an 80-fold increase in creatine phosphokinase (CK) activity which was largely accounted for by a similar increase in the amount of CK mRNA [4].
• Creatine kinase (CK; EC 2.7.3.2) plays an important role in energy metabolism in brain and muscle [5].
• To define the structures of canine CK isoenzymes and to elucidate the mechanism of regulation in their expression, CK cDNA clones from dog myocardium were isolated [5].
• Activation of PKCepsilon by phorbol 12-myristate 13-acetate or H(2)O(2) resulted in mitoK(ATP)-independent inhibition of MPT opening, whereas activation of PKCepsilon by PKG or the specific PKCepsilon agonist psiepsilon receptor for activated C kinase caused mitoK(ATP)-dependent inhibition of MPT opening [6].

Biological context of Chka

• In contrast, the A- and C-kinase inhibitors prevented both LH and GnRH induction of granulosa cell luteinization [7].
• At short times of incubation with 1 mM Cch, a concentration which maximally activates PI metabolism, increased phosphorylation of a group of synaptosomal proteins, including B-50 and myristoylated, alanine-rich C kinase substrate (MARCKS), was observed [8].
• Interaction of protein kinase C with RACK1, a receptor for activated C-kinase: a role in beta protein kinase C mediated signal transduction [9].
• H-7, a C kinase inhibitor, did not inhibit either chemotaxis or SMC adhesion at 100 mumol/L [10].
• A homology comparison with the previously reported choline kinase cDNAs (CKR1 and CKR2) from rat liver showed 66%-68% in entire nucleotide sequences and 57%-59% in amino acid sequences, indicating that the cloned cDNA here must be a novel CK/EK gene product [11].

Anatomical context of Chka

• Taken together, these results provide biological evidence that the response of granulosa cells to the LH surge appears to involve the activation of A- and C-kinase pathways [7].
• Whereas specific CK activity did not change significantly in axotomized SCG, in which the ratio of glial cells to neurons is greatly increased for a week after the operation., it was remarkably increased after denervation, in which the preganglionic cholinergic nerve terminals had degenerated [12].
• The activities of choline kinase (CK) and choline acetyltransferase (ChAT) were examined in vitro in superior cervical sympathetic ganglia (SCG) excised from rats following aerobic incubation for 1 h in a medium containing various choline concentrations, with and without application of a high KCl level (70 mM) [12].
• Furthermore, when coupled with recent data on the plasticity of LECs, the present findings provide the first essential element in our definition of the signaling pathway(s) that link growth/differentiation events with CK gene regulation in typical simple epithelial cells [13].
• These findings suggest the induction of Mn-SOD by TSH in thyroid cells and point to a role of C-kinase in this process, thereby indicating that a close relationship exists between the serum TSH level and the change in Mn-SOD content in thyrocytes with thyroid dysfunction [14].

Associations of Chka with chemical compounds

• Ganglionic CK activity was strongly inhibited (by approximately 75%) at low extracellular choline concentrations (1-5 microM) but rose as the choline concentration was raised to 10-50 microM in the incubation medium, then fell and rose again with further increases in choline concentration [12].
• Aldosterone lowers protein kinase C (PKC) activity in myocyte-enriched cultures from neonatal Sprague-Dawley rat hearts, with activity measured by the transfer of phosphate to myristolated alanine-rich C-kinase substrate, in the presence of Ca2+, phosphatidylserine, and diolein [15].
• The increase in CKB protein during cerebellar postnatal development was coincident with that of the ubiquitous mitochondrial CK protein and mRNA, indicating that a functional phosphocreatine energy shuttle probably exists for efficient ATP regeneration in the cerebellum [16].
• When either a high KCl level or hemicholinium-3 (HC-3; 50 microM) was added to the medium in the presence or absence of choline, ganglionic CK activity was markedly inhibited [12].
• A similar but moderate accelerative effect on ganglionic CK activity was also observed after addition of acetylcholine (ACh; 1 mM) without eserine [12].

Other interactions of Chka

• RACK (receptor for activated C-kinase) is a protein that binds and translocates protein kinase C (PKC) to the appropriate cellular organelles [17].
• Luteinizing hormone induces prostaglandin endoperoxide synthase-2 and luteinization in vitro by A-kinase and C-kinase pathways [7].
• Different inhibitors, such as cAMP phosphodiesterase inhibitor OPC3689, calmodulin inhibitor W-7, and C-kinase inhibitor H-7, were tested in isolated hepatocytes to determine whether intracellular signal transduction systems are involved in the liver cell injury produced by A23187 [18].

Analytical, diagnostic and therapeutic context of Chka

• Southern blot analysis suggests that a CK gene family exists [5].
• Diltiazem reduced leakage of creatine (CK) kinase during the first 15 min of reperfusion from 102 +/- 8 IU/15 min/g dry wt to 67 +/- 9 IU/15 min/g dry wt (P less than 0.05) [19].
• However, during the subsequent period of diltiazem-free perfusion, CK leakage was similar to control values (131 +/- 24 vs 142 +/- 34 IU/45 min/g dry wt, respectively) [19].
• After 1 h of reperfusion there was no significant difference in total CK leakage between the diltiazem and the control groups (198 +/- 32 vs 244 +/- 39 IU/60 min/g dry wt, respectively) [19].
• Immunoelectron microscopy clearly demonstrated that CK-positive osteoclast-lineage cells made contact with mesenchymal cells with prominent nucleoli and well-developed cell organelles [20].

References