The changes of protein kinase C activity in peripheral blood lymphocytes in the patients with obstructive jaundice and the implication

2001 ◽  
Vol 21 (2) ◽  
pp. 119-121
Author(s):  
Wang Jianming ◽  
Zou Qian ◽  
Zou Shengquan
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Obstructive Jaundice ◽  
Peripheral Blood ◽  
Peripheral Blood Lymphocytes ◽  
Blood Lymphocytes ◽  
Kinase C ◽  
Protein Kinase C Activity

scholarly journals Regularities of endogenous lipid metabolites formation in phorbol 12-miristate 13-acetate-stimulated peripheral blood lymphocytes at leukemia

2011 ◽  
Vol 57 (4) ◽  
pp. 420-428
Author(s):  
T.B. Batikyan ◽  
G.V. Hakopyan ◽  
M.P. Lazyan ◽  
T.P. Torgomyan ◽  
R.A. Kazaryan ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Palmitic Acid ◽  
Peripheral Blood ◽  
Peripheral Blood Lymphocytes ◽  
Biologically Active ◽  
Leukemic Cells ◽  
Blood Lymphocytes ◽  
Kinase C ◽  
Lipid Metabolites

Regularities of biologically active lipid metabolites formation in dynamics (5, 10, 30, 60 s) by phorbol 12-miristate 13-acetate stimulation in [14C]palmitic acid have been investigated in normal and leukemia peripheral blood lymphocytes prelabeled with [14C]palmitate. In normal cells there was two-phase formation of 1,2-diacylglycerol (5, 30 s), lysophosphatidylcholine (10, 60 s), as well as free palmitic acid at 10 s of stimulation. Under the identical experimental conditions there was inhibition of investigated lipid release processes at early (5 and 10 s) stages of stimulation of leukemic lymphocytes. At later (30, 60 s) terms of these lymphocytes the activation, basically, similar to norm changes in the formation of palmitic acid-containing metabolites except free palmitic acid (the level of which raised only at 60 second of the post-stimulation) was found. Various protein kinases C are involved in the regulation of investigated lipid levels at certain stages of signal transduction both in norm, and in blast cells. Short-term (5, 10 s) activations of healthy donors lymphocytes are coupled to functioning of Са2+-independent isoforms of protein kinase C. The inhibition of this protein kinase C in leukemic cells leads to normalization of the investigated lipid release. The data obtained suggests disorders of early membrane-bound reactions in agonist - and a protein kinase C-mediated processes of formation palmitic acid-containing lipid metabolites in the leukemic cells in comparison with the norm.

Cyclosporine inhibits protein kinase C-dependent signals in human peripheral blood lymphocytes

1989 ◽  
Vol 46 (4) ◽  
pp. 292-295 ◽  
Author(s):  
Marvin A. McMillen ◽  
Harold A. Schaefer ◽  
John D. MacArthur ◽  
Thomas A. Adrian ◽  
Irvin M. Modlin
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Peripheral Blood ◽  
Human Peripheral Blood ◽  
Peripheral Blood Lymphocytes ◽  
Blood Lymphocytes ◽  
Human Peripheral Blood Lymphocytes ◽  
Kinase C

Chronic treatment by the calcium channel blocker ± PN 200-110 in the rat counteracts the stimulations of pituitary weight, prolactin release and pituitary C-kinase activity induced by a chronic estradiol treatment, in vivo

1990 ◽  
Vol 122 (3) ◽  
pp. 403-408
Author(s):  
Ph. Touraine ◽  
P. Birman ◽  
F. Bai-Grenier ◽  
C. Dubray ◽  
F. Peillon ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Plasma Prolactin ◽  
Estradiol Treatment ◽  
Kinase C ◽  
Protein Kinase C Activity

Abstract In order to investigate whether a calcium channel blocker could modulate the protein kinase C activity in normal and estradiol pretreated rat pituitary, female Wistar rats were treated or not (controls) with ± PN 200-110 (3 mg · kg−1 · day−1, sc) for 8 days or with estradiol cervical implants for 8 or 15 days, alone or in combination with PN 200-110 the last 8 days. Estradiol treatment induced a significant increase in plasma prolactin levels and pituitary weight. PN 200-110 administered to normal rats did not modify these parameters, whereas it reduced the effects of the 15 days estradiol treatment on prolactin levels (53.1 ± 4.9 vs 95.0 ±9.1 μg/l, p<0.0001) and pituitary weight (19.9 ± 0.4 vs 23.0 ± 0.6 mg, p <0.001), to values statistically comparable to those measured after 8 days of estradiol treatment. PN 200-110 alone did not induce any change in protein kinase C activity as compared with controls. In contrast, PN 200-110 treatment significantly counteracted the large increase in soluble activity and the decrease in the particulate one induced by estradiol between day 8 and day 15. We conclude that PN 200-110 opposed the stimulatory effects of chronic in vivo estradiol treatment on plasma prolactin levels and pituitary weight and that this regulation was related to a concomitant modulation of the protein kinase C activity.

Swainsonine Modulation of Protein Kinase C Activity in Murine Peritoneal Macrophages

1990 ◽  
Vol 2 (10) ◽  
pp. 333-338 ◽  
Author(s):  
Pascal Breton ◽  
Amha Asseffa ◽  
Krzysztof Grzegorzewski ◽  
Steven K. Akiyama ◽  
Sandra L. White ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Peritoneal Macrophages ◽  
Kinase C ◽  
Protein Kinase C Activity ◽  
Murine Peritoneal Macrophages
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