Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.11.1 (protein kinase)
81,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bilateral occlusion of common carotid arteries in Mongolian gerbils was produced for the periods (up to 15 min) which were shown to be totally reversible. There was an initial increase of cyclic AMP and GABA levels and enhanced activities of adenylate cyclase and glutamate decarboxylase, as well as the reduction of norepinephrine level and decreased activities of monoamine oxidase, GABA-transaminase and Na+-K+-ATPase. Following these changes, decreased concentration of dopamine, serotinin and glutamate were found. The activities of total protein kinase and acetylcholinesterase were found to be reduced after longer periods of short-term ischemia. The data are consistent with the concept of increased non-controled release of putative neurotransmitters in ischemia.
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PMID:Alterations of putative neurotransmitters and enzymes during ischemia in gerbil cerebral cortex. 3 75

Dopa-decarboxylase, acetylcholinesterase, sodium plus potassium stimulated adenosine triphosphatase (Na+ + K+-ATPase), and membrane-bound protein kinase were compared in the erythrocytes of patients with Huntington's disease and normal controls. All these enzymes also exist in the basal ganglia. The Na+ +K+-ATPase level was elevated (p less than 0.05) in Huntington's disease, while no significant changes were observed in the other enzymes. This finding is consistent with the concept that Huntington's disease is associated with a general membrane abnormality.
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PMID:Increased sodium plus potassium adenosine triphosphatase activity in erythrocyte membranes in Huntington's disease. 21 30

Retinoic acid (RA) induced neuronal differentiation in A126-1B2 cells and 123.7 cells, two mutant lines of PC12 that are deficient in cAMP-dependent protein kinase, but not in the parental PC12 cell line. A single exposure to RA was sufficient to cause neurite formation and inhibit cell division for a period of greater than 3 wk, suggesting that RA may cause a long-term, stable change in the state of these cells. In A126-1B2 cells, RA also induced the expression of other markers of differentiation including acetylcholinesterase and the mRNAs for neurofilament (NF-M) and GAP-43 as effectively as nerve growth factor (NGF). Neither NGF nor RA stimulated an increase in the expression of smg-25A in A126-1B2 cells, suggesting that the cAMP-dependent protein kinases may be required for an increase in the expression of this marker. RA also caused a rapid increase in the expression of the early response gene, c-fos, but did not effect the expression of egr-1. RA equivalently inhibited the division of A126-1B2 cells, 123.7 cells and parental PC12 cells, so RA induced differentiation is not an indirect response to growth arrest. In contrast, the levels of retinoic acid receptors (RAR alpha and RAR beta), and retinoic acid binding protein (CRABP) mRNA were strikingly higher in both A126-1B2 cells and 123.7 cells than in the parental PC12 cells. The deficiencies in cAMP-dependent protein kinase may increase the expression of CRABP and the RARs; and, thus, cAMP may indirectly regulate the ability of RA to control neurite formation and neural differentiation. Thus, RA appears to regulate division and differentiation of PC12 cells by a biochemical mechanism that is quite distinct from those used by peptide growth factors.
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PMID:Retinoic acid stimulates the differentiation of PC12 cells that are deficient in cAMP-dependent protein kinase. 164 38

Mouse C1 line cells are megakaryoblastic cells established by coinfection of Abelson murine leukemia virus and recombinant simian virus 40. We examined the effects of various compounds on growth and differentiation of these cells. Megakaryocytic differentiation of C1 cells was not induced by cytokines that stimulate megakaryocytic maturation of normal progenitor cells, such as interleukin 3 and 6 and granulocyte-macrophage colony-stimulating factor. However, the cells were induced to differentiate into megakaryocytes by treatment with some protein kinase inhibitors. The inhibition of v-abl tyrosine kinase activity preceded induction of differentiation of the cells treated with tyrosine kinase inhibitors such as genistein, herbimycin A, and erbstatin. Treatment of C1 cells with a v-abl antisense oligomer inhibited their proliferation and induced acetylcholinesterase activity, a typical marker of megakaryocytic differentiation. These results suggest that inhibition of v-abl function is associated with induction of megakaryocytic differentiation of C1 cells. Among the compounds tested, 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7), a potent inhibitor of cyclic nucleotide-dependent and Ca(2+)-phospholipid-dependent (protein kinase C) protein kinases, was the most potent inducer of differentiation of C1 cells. However, the differentiation-inducing effect of H-7 was unlikely to be mediated through inhibition of protein kinase C or cyclic nucleotide-dependent kinases, because other types of inhibitors of these kinases were not effective, and a protein kinase activator (phorbol ester) induced differentiation of C1 cells. Moreover, neither v-abl mRNA expression nor v-abl kinase activity in C1 cells was affected by treatment with H-7. These findings indicate that induction of megakaryocytic differentiation by H-7 is not related to inhibition of v-abl kinase, but rather to some novel function of H-7.
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PMID:Induction by some protein kinase inhibitors of differentiation of a mouse megakaryoblastic cell line established by coinfection with Abelson murine leukemia virus and recombinant SV40 retrovirus. 165 10

Sarcolemmal membranes were isolated from porcine skeletal muscle by modifications of a LiBr-extraction technique. Latency determinations of acetylcholinesterase, ouabain-sensitive p-nitrophenylphosphatase, [3H]ouabain binding, and (Na+ + K+)-ATPase activities indicated that 65-76% of the membranes were sealed inside-out vesicles. The preparations were enriched in cholesterol and phospholipid, and demonstrated adenylate cyclase activity and both cAMP and cGMP phosphodiesterase activities. An indication of the purity of this fraction was that the Ca2+-ATPase activity (0.13 mumol Pi mg-1 min-1 at 37 degrees C) was 3.8% of that of porcine skeletal muscle sarcoplasmic reticulum preparations. Pertussis toxin specifically catalyzed the ADP-ribosylation of a Mr 41,000 sarcolemmal protein, indicating the presence of the inhibitory guanine nucleotide regulatory protein of adenylate cyclase, Ni. An endogenous ADP-ribosyltransferase activity, with several membrane protein substrates, was also demonstrated. The addition of exogenous cAMP-dependent protein kinase or calmodulin promoted the phosphorylation of a number of sarcolemmal proteins. The calmodulin-dependent phosphorylation exhibited an approximate K 1/2 for Ca2+ of 0.5 microM, and an approximate K 1/2 for calmodulin of 0.1 microM. 125I-Calmodulin affinity labeling of the sarcolemma, using dithiobis(succinimidyl propionate), demonstrated the presence of Mr 160,000 and 280,000 calmodulin-binding components in these membranes. These results demonstrate that this porcine preparation will be valuable in the study of skeletal muscle sarcolemmal ion transport, protein and hormonal receptors, and protein kinase-catalyzed phosphorylation.
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PMID:Components of purified sarcolemma from porcine skeletal muscle. 299 26

Focal degenerative changes of skeletal muscle fibers (decrease in mean diameter, excessive axonal branching and a decrease in the mean diameter of motor end-plates together with a reduction of their acetylcholinesterase levels) were found by means of the experimental model thyrotoxic myopathy in mice compared to controls. A decrease in protein kinase affinity to cAMP and an increase in the number of nucleotide binding sites were revealed with a simultaneous decrease in cAMP level. The weakening of hormonal control of cAMP-dependent processes is probably the basic cause of muscular weakness and structural changes in skeletal muscles in thyrotoxic myopathy.
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PMID:Pathogenesis of experimental thyrotoxic myopathy. 300 98

We have characterized and quantitated the level of cAMP-dependent protein kinase in the NS-20, N1E-115, N-18 and N1A-103 mouse neuroblastoma clonal cell lines, and we have correlated the occurrence of functional cAMP-dependent protein kinase with the dibutyryl cAMP-induced differentiated functions in these cells. Our results demonstrate the presence of functional cAMP-dependent protein kinase in extracts of all four cell lines examined, including the 'neurite minus' N1A-103 cell line. Dibutyryl cAMP induced neurite outgrowth and acetylcholinesterase activity in the NS-20, N1E-115 and N-18 neuroblastoma cell lines, but not in the N1A-103 cell line. However, dibutyryl cAMP caused a 2-3-fold increase in the R1 regulatory subunit protein and cAMP-phosphodiesterase activity in the 'neurite minus' N1A-103 cells in a manner similar to that of the other three 'neurite positive' cell lines. These results suggest that the biochemical lesion(s) subserving the neurite-minus phenotype of the N1A-103 cells may be distal to the activation of cAMP-dependent protein kinase and is in a biochemical pathway distinct from the induction of R1 regulatory subunit protein and cAMP-phosphodiesterase activity.
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PMID:Identification of functional cAMP-dependent protein kinase in a 'neurite minus' mouse neuroblastoma cell line. 303 79

Neurochemical investigations of the whole temporal lobe of cases with Alzheimer's disease (n = 15); 80.7 +/- 1.7 yr), Pick's disease (n = 3; 65 +/- 1.7 yr), and age-matched controls (n = 18; 74.7 +/- 2.6 yr), demonstrate that Alzheimer's and Pick's disease are primary degenerative brain diseases. The activities of glycolytic enzymes, ATPases, carbonic anhydrase, acetylcholinesterase and protein kinase were significantly lower in Alzheimer's and in Pick's disease than in age-matched controls. Pick's disease is characterised by a more pronounced reduction of the enzymes investigated, which is considered to be an expression of a more dramatic degenerative process. The differences between Alzheimer's disease and Pick's disease are quantitative.
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PMID:Neurochemical enzyme changes in Alzheimer's and Pick's disease. 608 77

The data obtained in mice with experimental thyrotoxic myopathy included a decrease in the median diameter of the muscle fibers by 17.1 per cent and various focal degenerative changes in less than 20 per cent of the muscle fibers; a statistically significant elevation in the activity of alpha-glycerophosphate dehydrogenase, as well as a reduction in phosphorylase activity and glycogen levels. There was also a significant diminution in the median diameter of the motor terminal plates, a decrease in cholinesterase activity and intensified collateral ramification of the distal axons. The major cause of the muscular weakness and structural changes in the skeletal muscles in thyrotoxic myopathy seems to lie in lowered cAMP concentrations and a weakened cAMP-dependent regulation of protein kinase.
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PMID:[Pathogenesis of experimental thyrotoxic myopathy]. 624 Aug 78

The expression of a adenosine cyclic 3':5'-monophosphate (cAMP)-binding protein, regulatory subunit of the type I cAMP-dependent protein kinase (Rl), and its functional significance in the differentiation of N-18 mouse neuroblastoma cells were examined. 8-Azidoadenosine cyclic 3':5'-[32P]monophosphate, a photoaffinity-labeling analog of cAMP, and high-resolution sodium dodecyl sulfate-polyacrylamide gel electrophoresis were used to identify and quantitate cAMP-binding proteins in cell extracts. The induction of differentiation of N-18 mouse neuroblastoma cells, initiated either by adding dibutyryl adenosine cyclic 3':5'-monophosphate to the growth medium or by culturing cells in medium supplemented with 1% fetal calf serum, led to a 3-fold increase in the amount of 8-azidoadenosine cyclic 3':5'-[32P]monophosphate incorporated into Rl, when assayed in vitro. This increased incorporation was attributable to an increase in the amount of Rl rather than to an increase in the affinity of Rl for 8-azidoadenosine cyclic 4':5'-[32P]monophosphate. The subunit molecular weight, isoelectric point, and immunoreactivity of Rl were found to be identical to that of the regulatory subunit of the type I cAMP-dependent protein kinase purified from bovine skeletal muscle. The increase in Rl was not accompanied by an increase in the cAMP-dependent protein kinase activity. DEAE-cellulose column chromatography confirmed the induction of Rl as a free cAMP-binding protein in the differentiated neuroblastoma cells. The possibility of a growth-dependent regulation of Rl was also examined. Addition of 2% dimethyl sulfoxide to cultures of N-18 mouse neuroblastoma cells inhibited cell growth without increasing the specific activity of Rl. Dimethyl sulfoxide had no effect on neurite outgrowth or acetylcholinesterase activity, two parameters characteristic of differentiated cells. The fact that the induction of Rl coincided with differentiation of the neuroblastoma cells suggests that the expression of Rl may be used as a biochemical index of differentiation in these cells. The presence of a free cAMP-binding protein, not associated with cAMP-dependent protein kinase in neuroblastoma cells, raises important considerations concerning the action of cAMP in the regulation of growth and differentiation.
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PMID:Induction of the regulatory subunit of type I adenosine cyclic 3':5'-monophosphate-dependent protein kinase in differentiated N-18 mouse neuroblastoma cells. 627 81


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