Ca(2+)‐induced Ca2+ release in myocytes from dyspedic mice lacking the type‐1 ryanodine receptor.
Ca(2+)‐induced Ca2+ release in myocytes from dyspedic mice lacking the type‐1 ryanodine receptor.
复制标题
Ca(2+) 诱导缺乏 1 型兰尼碱受体的运动不良小鼠的肌细胞中 Ca2+ 释放。
作者：
H. Takeshima;T. Yamazawa;T. Ikemoto;Hiroaki Takekura;M. Nishi;Tetsuo Noda;M. Iino
虽然ryanodine受体（RyR）的亚型1和2作为细胞内Ca2+释放通道发挥作用，但对首次在大脑中发现的第三亚型（RyR‐3）的功能知之甚少。来自小鼠的纯合RyR‐1基因靶向突变的肌细胞（不良小鼠）现在可以用于研究RyR‐3的功能，根据我们的逆转录-聚合酶链式反应分析，RyR‐3主要在这些细胞中表达。我们在这里证明，在这些肌细胞中，咖啡因-，ryanodine -和腺嘌呤核苷酸敏感的Ca(2+) -诱导的Ca2+释放对Ca2+的敏感性比RyR - 1低约10倍。虽然RyR‐3不介导骨骼肌类型的兴奋-收缩耦合，但我们认为RyR‐3可能诱导细胞内Ca2+释放，以响应高阈值的Ca2+上升。
While subtypes 1 and 2 of the ryanodine receptor (RyR) function as intracellular Ca2+ release channels, little is known about the function of the third subtype (RyR‐3), first identified in brain. Myocytes from mice homozygous for a targeted mutation in the RyR‐1 gene (dyspedic mice) can now be used for a study on the function of RyR‐3, which is predominantly expressed in these cells according to our reverse transcription‐polymerase chain reaction analysis. We here demonstrate in these myocytes caffeine‐, ryanodine‐ and adenine nucleotide‐sensitive Ca(2+)‐induced Ca2+ release with approximately 10 times lower sensitivity to Ca2+ than that of RyR‐1. Although RyR‐3 does not mediate excitation‐contraction coupling of the skeletal muscle type, we propose that RyR‐3 may induce intracellular Ca2+ release in response to a Ca2+ rise with a high threshold.
鸡骨骼肌兰尼碱受体亚型：离子通道特性。
影响因子：
3.4
作者：
Percival,AL;Williams,AJ;Kenyon,JL;Grinsell,MM;Airey,JA;Sutko,JL
通讯作者：
Sutko,JL
30 S 龙虾骨骼肌 Ca2 释放通道（兰尼碱受体）具有与哺乳动物通道蛋白不同的功能特性。
DOI：
--
发表时间：
1992
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Seok,JH;Xu,L;Kramarcy,NR;Sealock,R;Meissner,G
通讯作者：
Meissner,G