Myosin-linked Calcium Regulation

1976 ◽  
pp. 122-136 ◽  
Author(s):  
J. Kendrick-Jones
Keyword(s):  
Calcium Regulation

Calcium regulation of phospholipase A2 is independent of calmodulin

1984 ◽  
Vol 121 (2) ◽  
pp. 507-513 ◽  
Author(s):  
Michael T. Withnall ◽  
Thomas J. Brown ◽  
Baljeet K. Diocee
Keyword(s):  
Phospholipase A2 ◽  
Calcium Regulation

DIFFERENCES IN PLATELET CALCIUM REGULATION BETWEEN AFRICAN AMERICANS AND CAUCASIANS

1994 ◽  
Vol 12 (2) ◽  
pp. 199???208 ◽  
Author(s):  
Masayuki Kimura ◽  
Jwa H. Cho ◽  
Norman Lasker ◽  
Abraham Aviv
Keyword(s):  
African Americans ◽  
Calcium Regulation

Corticosterone impairs hippocampal neuronal calcium regulation — possible mediating mechanisms

1993 ◽  
Vol 602 (1) ◽  
pp. 84-90 ◽  
Author(s):  
Elicia M. Elliott ◽  
Robert M. Sapolsky
Keyword(s):  
Calcium Regulation ◽  
Mediating Mechanisms

scholarly journals Myotubes from transgenic mdx mice expressing full-length dystrophin show normal calcium regulation.

1994 ◽  
Vol 5 (10) ◽  
pp. 1159-1167 ◽  
Author(s):  
W F Denetclaw ◽  
F W Hopf ◽  
G A Cox ◽  
J S Chamberlain ◽  
R A Steinhardt
Keyword(s):  
Single Channel ◽  
Calcium Regulation ◽  
Full Length ◽  
Mdx Mice ◽  
Free Calcium ◽  
Muscle Degeneration ◽  
Channel Activity ◽  
Mouse Muscle ◽  
Calcium Dependent ◽  
Normal Calcium

A lack of dystrophin results in muscle degeneration in Duchenne muscular dystrophy. Dystrophin-deficient human and mouse muscle cells have higher resting levels of intracellular free calcium ([Ca2+]i) and show a related increase in single-channel open probabilities of calcium leak channels. Elevated [Ca2+]i results in high levels of calcium-dependent proteolysis, which in turn increases calcium leak channel activity. This process could initiate muscle degeneration by further increasing [Ca2+]i and proteolysis in a positive feedback loop. Here, we tested the direct effect of restoration of dystrophin on [Ca2+]i and channel activity in primary myotubes from mdx mice made transgenic for full-length dystrophin. Transgenic mdx mice have been previously shown to have normal dystrophin localization and no muscle degeneration. Fura-2 calcium measurements and single-channel patch recordings showed that resting [Ca2+]i levels and open probabilities of calcium leak channels of transgenic mdx myotubes were similar to normal levels and significantly lower than mdx littermate controls (mdx) that lack dystrophin. Thus, restoration of normal calcium regulation in transgenic mdx mice may underlie the resulting absence of degeneration.

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