The influence of the lipid–protein interaction on the membrane dynamics

2004 ◽  
Vol 350 (1-3) ◽  
pp. E623-E626 ◽  
Author(s):  
F Natali ◽  
A Relini ◽  
A Gliozzi ◽  
R Rolandi ◽  
P Cavatorta ◽  
...  
Keyword(s):  
Protein Interaction ◽  
Membrane Dynamics ◽  
Lipid Protein Interaction

Preparation of Chloroplast Lipid Membrane and Lipid-protein Interaction Assay

BIO-PROTOCOL ◽  
2016 ◽  
Vol 6 (3) ◽  
Author(s):  
Kumiko Okazaki ◽  
Shin-ya Miyagishima ◽  
Hajime Wada
Keyword(s):  
Protein Interaction ◽  
Lipid Membrane ◽  
Lipid Protein Interaction

Effect of lipid-protein interaction on the color of bacteriorhodopsin

1989 ◽  
Vol 973 (2) ◽  
pp. 257-262 ◽  
Author(s):  
C. Pande ◽  
R. Callender ◽  
J. Baribeau ◽  
F. Boucher ◽  
A. Pande
Keyword(s):  
Protein Interaction ◽  
Lipid Protein Interaction

Arachidonic acid and its metabolites increase Cai in cultured rat oligodendrocytes

1993 ◽  
Vol 264 (3) ◽  
pp. C632-C640 ◽  
Author(s):  
B. Soliven ◽  
M. Takeda ◽  
T. Shandy ◽  
D. J. Nelson
Keyword(s):  
Spinal Cord ◽  
Arachidonic Acid ◽  
Linoleic Acid ◽  
Intracellular Calcium ◽  
Protein Interaction ◽  
Membrane Lipid ◽  
Rat Spinal Cord ◽  
Fura 2 ◽  
Fluorescence Measurements ◽  
Lipid Protein Interaction

Fluorescence measurements of intracellular calcium (Cai) were made on cultured rat spinal cord oligodendrocytes (OLGs) using the dye fura-2. Exposure of OLGs to arachidonic acid (AA) (5-50 microM) elicited a concentration-dependent increase in Cai that was derived mainly from extracellular Ca2+. AA at 50 microM also released Ca2+ from intracellular stores. The response to AA was not decreased by nifedipine or by inhibition of Na(+)-Ca2+ exchange. AA-induced Ca2+ influx pathway was permeable to Mn2+ and Co2+ but not to Ba2+ and was not markedly influenced by depolarization, suggesting that AA activates a voltage-independent, not strictly selective, Ca2+ channel. The Cai response to AA was partially attenuated in the presence of indomethacin, indicating that the Cai response was mediated in part by cyclooxygenase products of AA. However, the AA-induced Cai response far exceeded that induced by prostaglandins and was mimicked by linoleic acid. We conclude that AA modulates Cai of OLGs via two mechanisms: 1) indirectly via cyclooxygenase pathway and 2) directly via membrane lipid-protein interaction.

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