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Journal articles on the topic 'Proteinkinase'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

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1

Kunick, Conrad, and Ingo Ott. "Metallkomplexe als Proteinkinase-Hemmstoffe." Angewandte Chemie 122, no. 31 (2010): 5354–56. http://dx.doi.org/10.1002/ange.201002062.

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2

Maelicke, Alfred. "Proteinkinase A und Fettleibigkeit." Nachrichten aus Chemie, Technik und Laboratorium 44, no. 10 (1996): 1002. http://dx.doi.org/10.1002/nadc.19960441016.

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3

Yefimov, A. S., A. A. Serghiyenko, Z. D. Vorobets, and L. M. Serghiyenko. "Activities of membranebound proteinkinase c and red cell ATPases in diabetic angiopathy." Problems of Endocrinology 39, no. 1 (1993): 11–14. http://dx.doi.org/10.14341/probl11896.

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The activities of proteinkinase C, total, Mg2 and Na+, K+-dependent ATPases in red cell membranes were compared in 46 patients with insulin independent, 30 ones with insulin dependent diabetes mellitus with various degrees of vascular disorders, and in 17 patients with atherosclerosis with the predominant involvement of the main vessels of the lower limbs. Diabetes mellitus and the progress of vascular disorders were associated with a more marked depression of proteinkinase C, total and Na+, K+-dependent ATPase activities, this being particularly characteristic of the patients with insulin-ind

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4

Holthausen, Friederike. "Gezielte Hemmung der Proteinkinase BRAF." Info Onkologie 17, no. 4 (2014): 58. http://dx.doi.org/10.1007/s15004-014-0865-3.

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5

Freitag, Anne, and Stefan Laufer. "Proteinkinase-Inhibitoren: selektiv und wirksam." Nachrichten aus der Chemie 63, no. 4 (2015): 420–25. http://dx.doi.org/10.1002/nadc.201590121.

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6

Shcherbakov, A. M., E. S. Gershtein, O. A. Anurova, and N. E. Kushlinskii. "Activated Proteinkinase B in Breast Cancer." Bulletin of Experimental Biology and Medicine 139, no. 5 (2005): 608–10. http://dx.doi.org/10.1007/s10517-005-0357-4.

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7

Grüb, M., M. El-Wardani, J. Mielke, et al. "Proteinkinase C Isoformen in Hornhautepithel und -endothel." Klinische Monatsblätter für Augenheilkunde 223, no. 12 (2006): 952–56. http://dx.doi.org/10.1055/s-2006-927130.

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8

Siemer, S., G. Stalter, M. Ziegler, and O. G. Issinger. "Charakterisierung der Proteinkinase CK2 in menschlichen Nierentumoren." Aktuelle Urologie 27, no. 01 (1996): 1–5. http://dx.doi.org/10.1055/s-2008-1055555.

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9

Issing, W. J., and T. P. U. Wustrow. "Überexpression von Proteinkinase-C-Isoenzymen in menschlichen Tumorzellinien." Laryngo-Rhino-Otologie 70, no. 03 (1991): 146–50. http://dx.doi.org/10.1055/s-2007-998007.

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10

Hug, Hubert. "Proteinkinase C— Schlüsselenzym der Signalübertragung in eukaryotischen Zellen." Biologie in unserer Zeit 22, no. 6 (1992): 336–41. http://dx.doi.org/10.1002/biuz.19920220619.

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11

Siffert, W. "Na+/H+-Austausch und Thrombozytenaktivierung." Hämostaseologie 07, no. 06 (1987): 147–50. http://dx.doi.org/10.1055/s-0038-1660546.

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ZusammenfassungDie Stimulation von Thrombozyten mit Thrombin führt zur Erhöhung von pHi. Diese Alkalisierung des Zytoplasmas wird durch die Aktivität eines Na+/H+-Austauschers in der Plasmamembran bewirkt. Vermutlich katalysiert die Proteinkinase C die Phosphorylierung dieses Transportsystems. Die Erhöhung von pHi ist eine wichtige Voraussetzung für die IP3-induzierte Ca2+-Freisetzung aus intrazellulären Speichern und damit unerläßlich für die Thrombozytenaktivierung (Abb. 5).

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12

Munir, Muhammad, and Mikael Berg. "The multiple faces of proteinkinase R in antiviral defense." Virulence 4, no. 1 (2013): 85–89. http://dx.doi.org/10.4161/viru.23134.

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13

Lamers, Jos M. J., and Johanna T. Meij. "G-protein — Regulated phospholipase C — Proteinkinase C in myocardium." Journal of Molecular and Cellular Cardiology 22 (May 1990): S134. http://dx.doi.org/10.1016/0022-2828(90)91911-p.

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14

Mighorati, G., M. C. Pagliacci, F. D'Adamio, F. Crocicchio, I. Nicoletti, and C. Riccardi. "Glucocorticoid-induced dna fragmentation: Role of proteinkinase-c activity." Pharmacological Research 26 (September 1992): 5–9. http://dx.doi.org/10.1016/1043-6618(92)90574-u.

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15

Kunick, Conrad, and Anne-Marie Egert-Schmidt. "Die kurze Geschichte der Proteinkinase-Inhibitoren. Jung, kompetitiv, erfolgreich." Pharmazie in unserer Zeit 37, no. 5 (2008): 360–68. http://dx.doi.org/10.1002/pauz.200800277.

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16

Ivanova, Maria A., Arina D. Kokorina, Polina D. Timofeeva, et al. "Calcium Export from Neurons and Multi-Kinase Signaling Cascades Contribute to Ouabain Neuroprotection in Hyperhomocysteinemia." Biomolecules 10, no. 8 (2020): 1104. http://dx.doi.org/10.3390/biom10081104.

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Pathological homocysteine (HCY) accumulation in the human plasma, known as hyperhomocysteinemia, exacerbates neurodegenerative diseases because, in the brain, this amino acid acts as a persistent N-methyl-d-aspartate receptor agonist. We studied the effects of 0.1–1 nM ouabain on intracellular Ca2+ signaling, mitochondrial inner membrane voltage (φmit), and cell viability in primary cultures of rat cortical neurons in glutamate and HCY neurotoxic insults. In addition, apoptosis-related protein expression and the involvement of some kinases in ouabain-mediated effects were evaluated. In short i

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17

Arnold, Maren E., Wolfgang R. Dostmann, Jody Martin, et al. "SERCA2a-phospholamban interaction monitored by an interposed circularly permutated green fluorescent protein." American Journal of Physiology-Heart and Circulatory Physiology 320, no. 6 (2021): H2188—H2200. http://dx.doi.org/10.1152/ajpheart.00858.2020.

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This study describes the design and characterization of a novel biosensor that can visualize the interaction of SERCA2a and phospholamban (PLB). The biosensor combines SERCA2a, a circularly permutated green fluorescent protein, and PLB into one recombinant protein (SGP). Proteinkinase A activation results in phosphorylation of the PLB domain and is associated with a marked increase in the fluorescence yield to allow for real-time monitoring of the SERCA2a and PLB interaction in cells.

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18

Chaykovska, L., U. Hoff, A. Kusch, et al. "SOTRASTAURIN MEDIATED INHIBITION OF PROTEINKINASE AMELIORATES SEVERE POSTTRANSPLANT PRESERVATION INJURY." Transplantation Journal 90 (July 2010): 205. http://dx.doi.org/10.1097/00007890-201007272-00392.

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19

Schramm, Andrea, Philip Mueller-Thuemen, Timo Littmann, Manuela Harloff, Takeaki Ozawa, and Jens Schlossmann. "Establishing a Split Luciferase Assay for Proteinkinase G (PKG) Interaction Studies." International Journal of Molecular Sciences 19, no. 4 (2018): 1180. http://dx.doi.org/10.3390/ijms19041180.

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20

KOPP, R., and A. PFEIFFER. "Feedback regulation of muscarinic phosphoinositide response: a role for proteinkinase-C?" Acta Endocrinologica 120, no. 3_Suppl (1989): S200. http://dx.doi.org/10.1530/acta.0.120s200.

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21

Lang, Gabriele E., and Jürgen Kampmeier. "Die Bedeutung der Proteinkinase C in der Pathophysiologie der diabetischen Retinopathie." Klinische Monatsblätter für Augenheilkunde 219, no. 11 (2002): 769–76. http://dx.doi.org/10.1055/s-2002-36328.

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22

Bryantseva, S. A., E. S. Gavryushina, A. I. Yemets, et al. "MAST2-like proteinkinase from grape Vitis vinifera: Cloning of catalytic domain cDNA." Cytology and Genetics 44, no. 4 (2010): 227–32. http://dx.doi.org/10.3103/s0095452710040079.

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23

RASMUSSEN, HOWARD, CARLOS M. ISALES, ROBERTO CALLE, et al. "Diacylglycerol Production, Ca2+Influx, and ProteinKinase C Activation in Sustained Cellular Responses*." Endocrine Reviews 16, no. 5 (1995): 649–81. http://dx.doi.org/10.1210/edrv-16-5-649.

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24

Spencker, Torsten, Margarete Goppelt-Struebe, Wolfgang Keese, Klaus Resch, and Manfred Rimpler. "Klassische Synthese eines selektiven Peptid-Substrates für die Messung der Proteinkinase C." Liebigs Annalen der Chemie 1993, no. 3 (1993): 237–40. http://dx.doi.org/10.1002/jlac.199319930142.

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25

Chun-yan, He, Zhou Xin, Li Xiao-ming, Yu Hong, and Hong Jia-ling. "Activation of proteinkinase ERK mediates induction of macrophage MMP-12 by OxLDL." Wuhan University Journal of Natural Sciences 9, no. 1 (2004): 120–24. http://dx.doi.org/10.1007/bf02912732.

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26

Kiesecker, C., E. Zitron, D. Scherer, et al. "350 Inhibition of heteromeric Kir2.x channels by proteinkinase C dependent phosphorylation." EP Europace 7, Supplement_1 (2005): 71–72. http://dx.doi.org/10.1016/eupace/7.supplement_1.71-b.

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27

WEIGERT, CORA, ULRICH SAUER, KATRIN BRODBECK, ANDREAS PFEIFFER, HANS U. HÄRING та ERWIN D. SCHLEICHER. "AP-1 Proteins Mediate Hyperglycemia-Induced Activation of the Human TGF-β1 Promoter in Mesangial Cells". Journal of the American Society of Nephrology 11, № 11 (2000): 2007–16. http://dx.doi.org/10.1681/asn.v11112007.

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Abstract. Hyperglycemia-induced overproduction of the prosclerotic cytokine transforming growth factor-β1 (TGF-β1) has been implicated in the pathogenesis of diabetic nephropathy. Because high glucose and phorbol esters (PMA) increase TGF-β1 mRNA levels in mesangial cells, this study was designed to characterize these effects on the human TGF-β1 promoter activity. With the use of luciferase reporter gene constructs containing TGF-β1 5′-flanking sequence (from -453 to +11 bp) transfected into mesangial cells, it was found that 30 mM glucose induced a nearly twofold increase in TGF-β1 promoter a

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28

Uraz, A., E. Ayhan, B. Yildirim, E. Bariş, S. Pehlivan, and K. Eren. "Immunoexpression of p38 Mitogen-Activated Proteinkinase in Patients with Aggressive and Chronic Periodontitis." European Journal of Inflammation 11, no. 1 (2013): 33–41. http://dx.doi.org/10.1177/1721727x1301100104.

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29

Schöndorf, T., C. M. Kurbacher, M. Becker, M. Warm, H. Kolhagen та U. J. Göhring. "Heterogeneity of proteinkinase C activity and PKC-ζ expression in clinical breast carcinomas". Clinical and Experimental Medicine 1, № 1 (2001): 1–8. http://dx.doi.org/10.1007/pl00012236.

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30

Andrassy, M., S. Schiekofer, J. Chen, et al. "Endothelzellaktivierung bei Diabetes mellitus." Hämostaseologie 21, no. 04 (2001): 151–58. http://dx.doi.org/10.1055/s-0037-1619518.

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ZusammenfassungGefäßerkrankungen gelten als eine Hauptursache für die Morbidität und Mortalität von Patienten mit Diabetes mellitus. Klinische Studien zeigen, dass eine intensivierte Blutzuckerkontrolle die Entwicklung vaskulärer Spätschäden deutlich verlangsamt, sodass Hyperglykämie mittlerweile als ein wichtiger Faktor für die Enstehung von Gefäßveränderungen betrachtet wird. Verschiedene durch Hyperglykämie aktivierte Stoffwechselwege wie der Polyolstoffwechselweg, die Aktivierung der Proteinkinase C, die nicht-enzymatische Glykierung von Proteinen und Veränderungen im Redoxpotenzial beeinf

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31

Oseshnyk, Rodion A., Inna E. Ushal, Ekaterina V. Svetkina, et al. "Individual peculiarities in pharmacokinetics of antiblastomic drugs in healthy volunteers." Reviews on Clinical Pharmacology and Drug Therapy 15, no. 1 (2017): 48–52. http://dx.doi.org/10.17816/rcf15148-52.

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The data of inter-individual variations in pharmacokinetics of antiblastomic drugs from the group of tyrosine proteinkinase inhibitors (imatinib, gefitinib and nilotinib) and antiblastomic immune modulator lenalidomide in healthy volunteers by meams of HPLC-MS/MS were represented in the article. The concentrations of the drugs studied were measured in the volunteer blood serum. The indeces Cmax (maximal concentration and time reaching), Tmax (time covering maximal concentration measure), AUC0-t (squire under pharmaceutical curve) were processed by trapetias method, Cmax/AUC0-t as well as Kel (

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32

Rauber, Christoph, and Stefan Berger. "Saturation Transfer Difference NMR Studies of the Interaction of the Proteinkinase CK2 with Peptides." Protein & Peptide Letters 19, no. 9 (2012): 934–39. http://dx.doi.org/10.2174/092986612802084447.

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33

Duyster, Justus, Hiroyoshi Hidaka, Karl Decker та Peter Dieter. "Proteinkinase C β-isoform triggers the formation of prostanoids and superoxide in liver macrophages". Biochemical and Biophysical Research Communications 183, № 3 (1992): 1247–53. http://dx.doi.org/10.1016/s0006-291x(05)80324-9.

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34

Bischof, J., J. Richter, C. Ianes, et al. "Identifizierung und Charakterisierung von Mutationen der Proteinkinase CK1delta im colorektalen Karzinom und im Pankreaskarzinom." Zeitschrift für Gastroenterologie 56, no. 08 (2018): e297-e297. http://dx.doi.org/10.1055/s-0038-1668907.

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35

Minkwitz, J., and H. Himmerich. "Adipositasentwicklung und metabolische Veränderungen unter Psychopharmakotherapie." Adipositas - Ursachen, Folgeerkrankungen, Therapie 07, no. 04 (2013): 236–42. http://dx.doi.org/10.1055/s-0037-1618823.

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ZusammenfassungAdipositasentwicklung und metabolische Entgleisungen sind häufige Nebenwirkungen psychopharmakologischer Therapie mit Antipsychotika, Antidepressiva und Stimmungsstabilisierern. Die verschiedenen psychopharmakologischen Substanzen zeigen klare Unterschiede bezüglich ihres Einflusses auf das Körpergewicht. Diese Unterschiede können teilweise durch unterschiedliche Affinität zum histaminergen H1-Rezeptor erklärt werden. Im Hypothalamus bewirkt der antihistaminerge Effekt dieser Psychopharmaka eine Erhöhung der Aktivität der Adenosinmonophosphat-aktivierten Proteinkinase (AMPK), di

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36

Mareková, Martina, Jiřina Vávrová, Doris Vokurková, and Jaroslav Cerman. "Light-Induced Photoactivation of Hypericin Inhibits Cellular Growth in Pituitary Adenoma Cell Line AtT20/D16v-F2 (Hypericin Inhibits Cellular Growth of AtT20/D16v-F2)." Acta Medica (Hradec Kralove, Czech Republic) 44, no. 1 (2001): 7–13. http://dx.doi.org/10.14712/18059694.2019.80.

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Cultivation with 4-8 μmol/l hypericin (specific proteinkinase C inhibitor) activated by light induced high inhibition of the rate of HL-60 cell growth. When hypericin treated cells were not exposed to light growth inhibition was insignificant. Cultivation with light activated hypericin in concentration 16 μmol/l slightly inhibited growth rate of AtT20/D16v-F2 cells. AtT20/D16v-F2 cells did not proliferate in presence of light activated 32 μmol/l hypericin. Evidence of apoptosis was found in HL-60 cells treated with 1-8 μmol/l light activated hypericin, with maximum of apoptotic cells detected

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37

Greil, W., G. Niedernhuber, D. Stübner, and R. Gärtner. "Inhibition of cAMP formation by EGF in thyroid follicles is mediated by intracellular Ca++." Acta Endocrinologica 116, no. 1_Suppl (1987): S267—S269. http://dx.doi.org/10.1530/acta.0.114s267.

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Abstract. The mechanism of cAMP-inhibition by EGF was studied in isolated porcine thyroid follicles. EGF inhibited TSH-induced cAMP-formation maximally by 40%, this effect remained up to 1 h of pre-incubation. The calcium-ionophore A 23 187 also inhibited cAMP-formation, but its effect was relieved after 1 h. The phorbolester TPA had a biphasic influence on cAMP-formation, with a transient increase (5 min) before a sustained inhibition (60 min); the inhibitory effect was mimicked by the diacylglycerol 1-oleoyl-2-acetyl-glycerol. Exogenous arachidonic acid had only a small and transient inhibit

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38

Salzer, Isabella. "Excitation of rat sympathetic neurons via M1 muscarinic receptors involves proteinkinase C and chloride channels." Intrinsic Activity 1, Suppl. 1 (2013): A2.2. http://dx.doi.org/10.25006/ia.1.s1-a2.2.

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39

Raab, Marc S., Klaus Podar, Jing Zhang, et al. "Targeting Proteinkinase C Alters ER-Stress and b-Catenin Signaling in Multiple Myeloma: Therapeutic Implications." Blood 110, no. 11 (2007): 258. http://dx.doi.org/10.1182/blood.v110.11.258.258.

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Abstract We have previously shown that the novel orally available small molecule inhibitor of PKC enzastaurin (Eli Lilly and Company) inhibits MM cell growth, survival and angiogenesis both in vitro and in vivo. To date, however, the downstream effects contributing to growth inhibition and cell death remain to be determined. Here, we performed global gene expression profiling on enzastaurin treated MM cells and identified 200 Genes to be differentially regulated with a &gt; 2-fold cut off. Strikingly, two major groups of up-regulated probe sets were associated with either of two pathways -

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40

Orlova, E. M., M. A. Kareva, E. Iu Zakharova, et al. "Three cases of Carney complex in the children: clinical and molecular-genetic features of Carney complex in the children (the first description in Russia)." Problems of Endocrinology 58, no. 5 (2012): 50–56. http://dx.doi.org/10.14341/probl201258550-56.

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Carney complex is a rare autosomal dominant condition that manifests itself as a combination of lentiginosis, heart and skin myxomas, primary pigmented micronodular adrenocortical hyperplasia with ACTH-independent hypercorticism, calcifying Sertoli cell testicular tumours, schwannomas, thyroid and breast tumours, and other neoplasms. A total of 400 patients presenting with this pathology has thus far been described worldwide. 75% of the patients with Carney complex were found to have mutations in the gene encoding for the regulatory alpha-subunit of proteinkinase A (PRKARIA). The present paper

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41

Haller, Hermann, E. Baur, J. Fischer, C. Lindschau, P. Quass, and Armin Distler. "64. Glucose-induced proteinkinase C translocation desensitizes vascular smooth muscle cells for angiotensin II and vasopressin." Journal of Hypertension 9 (1991): S449. http://dx.doi.org/10.1097/00004872-199112006-00255.

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42

Haller, Hermann, E. Baur, J. Fischer, C. Lindschau, P. Quass, and Armin Distler. "64. Glucose-induced proteinkinase C translocation desensitizes vascular smooth muscle cells for angiotensin II and vasopressin." Journal of Hypertension 9, no. 6 (1991): S449. http://dx.doi.org/10.1097/00004872-199112000-00255.

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43

Hauschildt, Sunna, Ute Steffens, Luise Wagner-Roos, and Wolfgang G. Bessler. "Role of proteinkinase C and phosphatidylinositol metabolism in lipopeptide-induced leukocyte activation as signal transducing mechanism." Molecular Immunology 25, no. 11 (1988): 1081–86. http://dx.doi.org/10.1016/0161-5890(88)90141-1.

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44

Antonova, O. S., A. Y. Plekhanov, E. I. Petrova, S. Y. Reznik, and N. Z. Klyueva. "Structural modifications of NAP-22 in the brain of spontaneously hypertensive rats." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 17, no. 4 (2011): 342–46. http://dx.doi.org/10.18705/1607-419x-2011-17-4-342-346.

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Background. The spontaneously hypertensive rat (SHR) strain is the most common animal model both of hypertension and of cognitive impairment. SHR show genetically determined calcium homeostasis abnormality. Objective. To investigate protein metabolism disturbance and reveal the difference in the level of a major proteinkinase C substrate, NAP-22, between SHR and normotensive WKY strain. Design and methods. Our experiments were carried out on SHR and WKY rats. NAP-22 amount was examined in developing hippocampus and in parietal cortex by immunoblotting with anti-NAP-22 serum. Results. In all st

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45

Nakai, Masamichi, Taizo Taniguchi, Toshio Kawamata та ін. "Involvement of proteinkinase C in desensitization of chemotaxis induced by amyloid β (25-35)in murine microglia". Japanese Journal of Pharmacology 73 (1997): 112. http://dx.doi.org/10.1016/s0021-5198(19)44956-1.

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46

Ueda, Seigo, Mizuhiro Arima, Arisa Ono, Satoru Matsushita, Kizuku Kuramoto, and Rikuo Ochi. "Proteinkinase C(C-kinase) modulation of chloride (Cl−) channel of endothelial cells coupled to the morphological change." Journal of Molecular and Cellular Cardiology 24 (May 1992): 99. http://dx.doi.org/10.1016/0022-2828(92)90323-r.

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47

Steffens, Ute, Wolfgang Bessler, and Sunna Hauschildt. "B cell activation by synthetic lipopeptide analogues of bacterial lipoprotein bypassing phosphatidylinositol metabolism and proteinkinase C translocation." Molecular Immunology 26, no. 9 (1989): 897–904. http://dx.doi.org/10.1016/0161-5890(89)90146-6.

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48

BLASCHKE, F. "P1768 Cobalt increases adhesion of human vascular smooth muscle cells by proteinkinase C dependent activation of ?1-integrin." European Heart Journal 24, no. 5 (2003): 339. http://dx.doi.org/10.1016/s0195-668x(03)94906-2.

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49

Mikhaylova, I. N., N. M. Treshalina, I. Zh Shubina, I. V. Manina, M. V. Kiselevsky, and A. N. Lukashev. "Antitumor proteinkinase inhibitor imatinib may be regarded as a potential correcting agent for COVID-19 associated pulmonary fibrosis." Advances in Molecular Oncology 7, no. 4 (2021): 20–28. http://dx.doi.org/10.17650/2313-805x-2020-7-4-20-28.

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Imatinib mesilate (Glivec) is a well-known antitumor target inhibitor of protein tyrosine kinase, which is effective in different cancer types expressing Bcr / Abl and, in particular, in hemoblastosis. A higher interest to imatinib during the COVID-19 epidemic is explained by the fact that cancer patients are one of the COVID-19 risk groups. Moreover, imatinib target mechanism of action, which is effective in cancer, can have a high potential against the most severe COVID-19 complication such as the disease associated pulmonary fibrosis. COVID-19 associated interstitial pulmonary fibrosis deve

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50

Kawada, Tomie, Yutaka Yoshida, Mikio Nakazawa, Shoichi Imai, and Shigehiko Kataoka. "Activation of cyclic AMP (cAMP)-dependent proteinkinase and inotropic and chronotropic effects of 8-benzylthio-N6-substituted cAMP derivatives." Japanese Journal of Pharmacology 40 (1986): 237. http://dx.doi.org/10.1016/s0021-5198(19)59458-6.

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