Faculty Opinions recommendation of Lipid-protein interaction of the MscS mechanosensitive channel examined by scanning mutagenesis.

Author(s):  
Ian Booth
2006 ◽  
Vol 91 (8) ◽  
pp. 2874-2881 ◽  
Author(s):  
Takeshi Nomura ◽  
Masahiro Sokabe ◽  
Kenjiro Yoshimura

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

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

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

1993 ◽  
Vol 264 (3) ◽  
pp. C632-C640 ◽  
Author(s):  
B. Soliven ◽  
M. Takeda ◽  
T. Shandy ◽  
D. J. Nelson

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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