Log in

Relevant bibliographies by topics / Proteinkinasa / Journal articles

To see the other types of publications on this topic, follow the link: Proteinkinasa.

Journal articles on the topic 'Proteinkinasa'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Proteinkinasa.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

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 (February 15, 1993): 11–14. http://dx.doi.org/10.14341/probl11896.

Full text

Abstract:

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-independent diabetes and macrovascular disorders, inhibited activities of proteinkinase C and ATPases in red cell membranes in the course of diabetic vascular disorders progress evidence their contribution to the pathogenesis of diabetic angiopathy.

APA, Harvard, Vancouver, ISO, and other styles

2

Kunick, Conrad, and Ingo Ott. "Metallkomplexe als Proteinkinase-Hemmstoffe." Angewandte Chemie 122, no. 31 (June 29, 2010): 5354–56. http://dx.doi.org/10.1002/ange.201002062.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

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

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

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

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

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

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Kentrup, D., and S. Reuter. "Rho-assoziierte Proteinkinasen (ROCK)." Der Nephrologe 9, no. 5 (August 2014): 391–94. http://dx.doi.org/10.1007/s11560-014-0884-y.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

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 (May 2005): 608–10. http://dx.doi.org/10.1007/s10517-005-0357-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Laufer. "Targeting Proteinkinases: The Selectivity Problem." Scientia Pharmaceutica 77, no. 1 (2009): 165. http://dx.doi.org/10.3797/scipharm.oephg.21.pl-03.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Grüb, M., M. El-Wardani, J. Mielke, E. Reinthal, K. Bartz-Schmidt, J. Rohrbach, and J. Martin. "Proteinkinase C Isoformen in Hornhautepithel und -endothel." Klinische Monatsblätter für Augenheilkunde 223, no. 12 (December 2006): 952–56. http://dx.doi.org/10.1055/s-2006-927130.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

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

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

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

Full text

Abstract:

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).

APA, Harvard, Vancouver, ISO, and other styles

12

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

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

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

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Ivanova, Maria A., Arina D. Kokorina, Polina D. Timofeeva, Tatiana V. Karelina, Polina A. Abushik, Julia D. Stepanenko, Dmitry A. Sibarov, and Sergei M. Antonov. "Calcium Export from Neurons and Multi-Kinase Signaling Cascades Contribute to Ouabain Neuroprotection in Hyperhomocysteinemia." Biomolecules 10, no. 8 (July 24, 2020): 1104. http://dx.doi.org/10.3390/biom10081104.

Full text

Abstract:

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 insults, HCY was less potent than glutamate as a neurotoxic agent and induced a 20% loss of φmit, whereas glutamate caused a 70% decrease of this value. Subnanomolar ouabain exhibited immediate and postponed neuroprotective effects on neurons. (1) Ouabain rapidly reduced the Ca2+ overload of neurons and loss of φmit evoked by glutamate and HCY that rescued neurons in short insults. (2) In prolonged 24 h excitotoxic insults, ouabain prevented neuronal apoptosis, triggering proteinkinase A and proteinkinase C dependent intracellular neuroprotective cascades for HCY, but not for glutamate. We, therefore, demonstrated here the role of PKC and PKA involving pathways in neuronal survival caused by ouabain in hyperhomocysteinemia, which suggests existence of different appropriate pharmacological treatment for hyperhomocysteinemia and glutamate excitotoxicity.

APA, Harvard, Vancouver, ISO, and other styles

15

Arnold, Maren E., Wolfgang R. Dostmann, Jody Martin, Michael J. Previs, Bradley Palmer, Martin LeWinter, and Markus Meyer. "SERCA2a-phospholamban interaction monitored by an interposed circularly permutated green fluorescent protein." American Journal of Physiology-Heart and Circulatory Physiology 320, no. 6 (June 1, 2021): H2188—H2200. http://dx.doi.org/10.1152/ajpheart.00858.2020.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

16

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

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

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

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Neary, JT. "MAPK Cascades in Cell Growth and Death." Physiology 12, no. 6 (December 1, 1997): 286–93. http://dx.doi.org/10.1152/physiologyonline.1997.12.6.286.

Full text

Abstract:

Distinct signal transduction cascades comprised of at least three proteinkinases mediate cellular proliferation and differentiation, growth arrest, and programmed cell death. These cytosolic enzymes relay extracellular signals from cell surface to nucleus, leading to changes in gene expression. Signaling components of these cascades offer new possibilities for therapeutic strategies in tumorigenesis, inflammatory diseases, immunopotentiation, wound healing, and regeneration.

APA, Harvard, Vancouver, ISO, and other styles

21

Chaykovska, L., U. Hoff, A. Kusch, R. Catar, J. Pützer, F. Fuller, and D. Dragun. "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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Zalevskaya, Alsu Gafurovna, and Evgenia Mikhailovna Patrakeeva. "Metabolicheskaya regulyatsiya i tsAMF-zavisimaya proteinkinaza (AMRK): vrag ili soyuznik?" Diabetes mellitus 11, no. 4 (December 15, 2008): 12–17. http://dx.doi.org/10.14341/2072-0351-5582.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

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 (April 12, 2018): 1180. http://dx.doi.org/10.3390/ijms19041180.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

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

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

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

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Chaikuad, Apirat, Pierre Koch, Stefan A. Laufer, and Stefan Knapp. "Das Cysteinom der Proteinkinasen als Zielstruktur in der Arzneistoffentwicklung." Angewandte Chemie 130, no. 16 (February 2, 2018): 4456–70. http://dx.doi.org/10.1002/ange.201707875.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

WEIGERT, CORA, ULRICH SAUER, KATRIN BRODBECK, ANDREAS PFEIFFER, HANS U. HÄRING, and 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, no. 11 (November 2000): 2007–16. http://dx.doi.org/10.1681/asn.v11112007.

Full text

Abstract:

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 activity after 24 h of incubation in human and porcine mesangial cells. Stimulation by PMA was more effective (2.3-fold). Mutagenesis in either one of the two or both activating protein-1 (AP-1) binding sites abolished the high glucose and the PMA effect. Furthermore, addition of the AP-1 inhibitor curcumin obliterated the glucose response. Corresponding experiments revealed that the transcription factor stimulating protein 1 was not involved in mediating the glucose effect. The high glucose-induced TGF-β1 promoter activation was also prevented by inhibitors of protein kinase C and p38 mitogen-activated proteinkinase. Electrophoretic mobility shift assays with oligonucleotides containing one of the two AP-1 binding sites showed that glucose treatment markedly enhanced the binding activity of nuclear proteins of mesangial cells, particularly to box B. Supershift assays demonstrated that JunD and c-Fos were present in the protein-DNA complexes under control and hyperglycemic conditions. The functional and structural results show that glucose regulates human TGF-β1 gene expression through two adjacent AP-1 binding sites and gives rise to the involvement of protein kinase C and p38 mitogen-activated proteinkinase in hyperglycemia-induced TGF-β1 gene expression.

APA, Harvard, Vancouver, ISO, and other styles

28

Andrassy, M., S. Schiekofer, J. Chen, P. M. Humpert, L. Bai, B. Chen, E. Schleicher, P. P. Nawroth, and A. Bierhaus. "Endothelzellaktivierung bei Diabetes mellitus." Hämostaseologie 21, no. 04 (2001): 151–58. http://dx.doi.org/10.1055/s-0037-1619518.

Full text

Abstract:

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 beeinflussen und verstärken sich dabei gegenseitig. Eine mögliche gemeinsame Endstrecke aller durch Hyperglykämie bedingten zellulären Veränderungen ist die Erzeugung von reaktiven Sauerstoffmolekülen (ROIs) und von oxidativem Stress. Oxidativer Stress aktiviert den Transkriptionsfaktor NF-κB und in Folge die NF-κB-abhängige endotheliale Genexpression, die möglicherweise zur endothelialen Dysfunktion bei Diabetes mellitus beitragen kann.

APA, Harvard, Vancouver, ISO, and other styles

29

Bryantseva, S. A., E. S. Gavryushina, A. I. Yemets, P. A. Karpov, Ya B. Blume, Yu F. Drygin, and E. S. Nadezhdina. "MAST2-like proteinkinase from grape Vitis vinifera: Cloning of catalytic domain cDNA." Cytology and Genetics 44, no. 4 (August 2010): 227–32. http://dx.doi.org/10.3103/s0095452710040079.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

RASMUSSEN, HOWARD, CARLOS M. ISALES, ROBERTO CALLE, DOUGLAS THROCKMORTON, MATTHEW ANDERSON, JOSE GASALLA-HERRAIZ, and RICHARD McCARTHY. "Diacylglycerol Production, Ca2+Influx, and ProteinKinase C Activation in Sustained Cellular Responses*." Endocrine Reviews 16, no. 5 (October 1995): 649–81. http://dx.doi.org/10.1210/edrv-16-5-649.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

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 (March 15, 1993): 237–40. http://dx.doi.org/10.1002/jlac.199319930142.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

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 (January 2004): 120–24. http://dx.doi.org/10.1007/bf02912732.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Kiesecker, C., E. Zitron, D. Scherer, S. Kathofer, D. Thomas, V. A. W. Kreye, W. Schoels, and C. A. Karle. "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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

Oseshnyk, Rodion A., Inna E. Ushal, Ekaterina V. Svetkina, Ekaterina A. Kolobova, Yury V. Strukov, Gennady G. Rodionov, and Petr D. Shabanov. "Individual peculiarities in pharmacokinetics of antiblastomic drugs in healthy volunteers." Reviews on Clinical Pharmacology and Drug Therapy 15, no. 1 (March 15, 2017): 48–52. http://dx.doi.org/10.17816/rcf15148-52.

Full text

Abstract:

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 (elimination constant) and T1/2 (period of semielimination) according to individual signs. The significant individual variability revealed for imatinib, gefitinib and nilotinib in healthy volunteers indicates on necessity of therapeutic drug monitoring in patients treated with them to aim optimal dosing.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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), die eine integrative Funktion bezüglich orexigener und anorexigener Signale hat. Diese Aktivierung führt zur Steigerung von Appetit und Nahrungsaufnahme.Störungen im Glukose- und Fettstoffwechsel sind nicht nur eine Konsequenz der Veränderungen des Essverhaltens und des Körpergewichts. Zusätzlich tragen muskarinerge und bislang unbekannte zentrale und periphere Faktoren zu dieser metabolischen Problematik bei, die vor allem unter der Therapie mit Antipsychotika auftritt.Daher ist eine engmaschige Kontrolle des Körpergewichts und des Glukosebzw. Fettstoffwechsels bei diesen Patienten angezeigt.

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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 after 8 μmol/l light activated hypericin. Light activated hypericin induces both apoptosis and necrosis in dose and time dependent manners in HL-60 cells, but causes only necrosis in AtT20/D16v-F2 cells.

APA, Harvard, Vancouver, ISO, and other styles

37

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 (January 2013): 33–41. http://dx.doi.org/10.1177/1721727x1301100104.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

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

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

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 (August 1987): S267—S269. http://dx.doi.org/10.1530/acta.0.114s267.

Full text

Abstract:

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 inhibitory effect on cAMP-formation. We conclude, that EGF inhibits cAMP-formation by a raise of intracellular Ca++, as well as by the direct activation of proteinkinase C, indicating, that a phosphorylated product could be a mediator for the inhibition of adenylate cyclase.

APA, Harvard, Vancouver, ISO, and other styles

40

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 (July 1, 2012): 934–39. http://dx.doi.org/10.2174/092986612802084447.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

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

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Bischof, J., J. Richter, C. Ianes, F. Leithäuser, D. Henne-Bruns, M. Kornmann, and U. Knippschild. "Identifizierung und Charakterisierung von Mutationen der Proteinkinase CK1delta im colorektalen Karzinom und im Pankreaskarzinom." Zeitschrift für Gastroenterologie 56, no. 08 (August 2018): e297-e297. http://dx.doi.org/10.1055/s-0038-1668907.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Orlova, E. M., M. A. Kareva, E. Iu Zakharova, G. A. Poliakova, I. V. Poddubnyĭ, K. N. Tolstov, L. I. Shiriaeva, 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 (October 15, 2012): 50–56. http://dx.doi.org/10.14341/probl201258550-56.

Full text

Abstract:

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 presents three cases of Carney syndrome diagnosed in adolescents. Two new mutations in the PRKARIA gene were identified (c.1111_1112insC (pp.Q370fsX11) and c.1016T>A (p.339V>D)). One of the patients had adrenal adenoma. To the best of our knowledge, it is the first case of benign adrenal tumour greater than 2 cm in size in the patient with Carney complex.

APA, Harvard, Vancouver, ISO, and other styles

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 (August 28, 2011): 342–46. http://dx.doi.org/10.18705/1607-419x-2011-17-4-342-346.

Full text

Abstract:

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 studied age groups (5-30 days), the amount of NAP-22 (including both aggregated and non-aggregated NAP-22 forms) in SHR telencephalon was considerably higher than in control WKY strain rats. There was also a significant difference between rate of development during considered period in SHR and WKY rats. Conclusion. Our results demonstrate that calcium homeostasis alterations could result in both cardiovascular abnormalities and in the damage of central nervous system through NAP-22 dysregulation.

APA, Harvard, Vancouver, ISO, and other styles

45

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

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

Raab, Marc S., Klaus Podar, Jing Zhang, Giovanni Tonon, Johannes H. Fruehauf, Iris Breitkreutz, Boris K. Lin, Teru Hideshima, Dharminder Chauhan, and Kenneth C. Anderson. "Targeting Proteinkinase C Alters ER-Stress and b-Catenin Signaling in Multiple Myeloma: Therapeutic Implications." Blood 110, no. 11 (November 16, 2007): 258. http://dx.doi.org/10.1182/blood.v110.11.258.258.

Full text

Abstract:

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 > 2-fold cut off. Strikingly, two major groups of up-regulated probe sets were associated with either of two pathways - endoplasmatic reticulum (ER)-stress response or WNT-signaling. Importantly, MM cells, producing high levels of paraprotein, are highly susceptible to perturbation of ER function and protein folding. Moreover, PKC isoforms have been reported to directly regulate the canonical WNT pathway via phosphorylation of b-catenin (CAT), leading to its ubiquination and proteasomal degradation. Specifically, we fist evaluated the role of enzastaurin in mediating ER-stress in MM cells. The transcriptional up-regulation of genes involved in ER-stress (GADD153/CHOP, GADD34, ATF3), triggered by enzastaurin at 3h, was confirmed by western blot analysis, accompanied by induction of the molecular ER chaperone BiP/grp78, phosphorylation of eIF2a consistent with PERK activation, and up-regulation of p21. These events were preceded by an early (1h) increase of intracellular calcium levels, a hallmark of ER-stress, assessed by FLUO4 staining. These data suggest an important role of ER-stress response in the early growth inhibition of MM cells caused by enzastaurin. Second, we delineated effects of enzastaurin on WNT pathway in MM and other tumor cell lines. Upon enzastaurin treatment, CAT was dephosphorylated at Ser33, 37, 41 in a dose- and time-dependent manner in all cell lines tested (10 MM, 3 colon cancer, HeLa, as well as human embryonic kidney 293 cells). Consequently, accumulation of CAT occurred in both cytosolic and nuclear fractions of treated MM cells, associated with activated TOPflash LUC-reporter system, confirming nuclear transactivating activity. Specific inhibition of CAT by siRNA partially rescued HeLa, HEK 293, and MM cells from cell death induced by enzastaurin. Analysis of downstream target molecules revealed a CAT-dependent up-regulation of c-Jun, but not of c-Myc or Cyclin D1. c-Jun has been reported to stabilize p73, a pro-apoptotic p53-family member; CAT induction by enzastaurin led to p73 (but not p53) activation and was also abrogated by CAT-specific siRNA. In turn, specific knockdown of p73 by siRNA rescued cells from enzastaurin-induced apoptosis. Finally, ectopic overexpression of CAT in HeLa and MM cells induced c-Jun expression and p73 activation, followed by apoptotic cell death. Our studies therefore indicate that ER-stress response contributes to the immediate inhibition of proliferation by enzastaurin, followed by CAT accumulation leading to p73 activation, contributing to enzastaurin-mediated cell death. These findings provide a novel link between CAT and p53-family members. Moreover p73, which is only rarely mutated in human cancers, represents a novel therapeutic target in MM.

APA, Harvard, Vancouver, ISO, and other styles

47

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

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 (December 1991): S449. http://dx.doi.org/10.1097/00004872-199112000-00255.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

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 (November 1988): 1081–86. http://dx.doi.org/10.1016/0161-5890(88)90141-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Chaikuad, Apirat, Pierre Koch, Stefan A. Laufer, and Stefan Knapp. "Innenrücktitelbild: Das Cysteinom der Proteinkinasen als Zielstruktur in der Arzneistoffentwicklung (Angew. Chem. 16/2018)." Angewandte Chemie 130, no. 16 (March 9, 2018): 4517. http://dx.doi.org/10.1002/ange.201802502.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!