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Modulation of cardiac ryanodine receptor 2 by calmodulin

机译：钙调蛋白对心脏ryanodine受体2的调节

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摘要

The high-conductance intracellular calcium (Ca2+) channel RyR2 is essential for the coupling of excitation and contraction in cardiac muscle. Among various modulators, calmodulin (CaM) regulates RyR2 in a Ca2+-dependent manner. Here we reveal the regulatory mechanism by which porcine RyR2 is modulated by human CaM through the structural determination of RyR2 under eight conditions. Apo-CaM and Ca2+-CaM bind to distinct but overlapping sites in an elongated cleft formed by the handle, helical and central domains. The shift in CaM-binding sites on RyR2 is controlled by Ca2+ binding to CaM, rather than to RyR2. Ca2+-CaM induces rotations and intradomain shifts of individual central domains, resulting in pore closure of the PCB95 and Ca2+-activated channel. By contrast, the pore of the ATP, caffeine and Ca2+-activated channel remains open in the presence of Ca2+-CaM, which suggests that Ca2+-CaM is one of the many competing modulators of RyR2 gating.
机译：高传导性细胞内钙（Ca2 +）通道RyR2对于心肌中兴奋和收缩的耦合至关重要。在各种调节剂中，钙调蛋白（CaM）以Ca2 +依赖的方式调节RyR2。在这里，我们揭示了通过在八种条件下对RyR2进行结构测定，人CaM调节猪RyR2的调控机制。 Apo-CaM和Ca2 + -CaM结合到由手柄，螺旋域和中心域形成的细长裂缝中不同但重叠的位点。 RyR2上CaM结合位点的移动受Ca2 +与CaM而不是与RyR2的结合控制。 Ca2 + -CaM诱导单个中心域的旋转和域内移位，从而导致PCB95和Ca2 +激活通道的孔封闭。相反，在存在Ca2 + -CaM的情况下，ATP，咖啡因和Ca2 +激活通道的孔保持开放，这表明Ca2 + -CaM是RyR2门控的许多竞争性调节剂之一。

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  • 来源
    《Nature》 |2019年第7769期|347-351|共5页
  • 作者

    Gong Deshun; Chi Ximin; Wei Jinhong; Zhou Gewei; Huang Gaoxingyu; Zhang Lin; Wang Ruiwu; Lei Jianlin; Chen S. R. Wayne; Yan Nieng;

  • 作者单位

    Tsinghua Univ, Sch Life Sci, Tsinghua Peking Joint Ctr Life Sci, Beijing Adv Innovat Ctr Struct Biol, Beijing, Peoples R China;

    Tsinghua Univ, Sch Life Sci, Tsinghua Peking Joint Ctr Life Sci, Beijing Adv Innovat Ctr Struct Biol, Beijing, Peoples R China;

    Univ Calgary, Libin Cardiovasc Inst Alberta, Dept Physiol & Pharmacol, Calgary, AB, Canada;

    Tsinghua Univ, Sch Life Sci, Tsinghua Peking Joint Ctr Life Sci, Beijing Adv Innovat Ctr Struct Biol, Beijing, Peoples R China;

    Tsinghua Univ, Sch Life Sci, Tsinghua Peking Joint Ctr Life Sci, Beijing Adv Innovat Ctr Struct Biol, Beijing, Peoples R China;

    Univ Calgary, Libin Cardiovasc Inst Alberta, Dept Physiol & Pharmacol, Calgary, AB, Canada;

    Univ Calgary, Libin Cardiovasc Inst Alberta, Dept Physiol & Pharmacol, Calgary, AB, Canada;

    Tsinghua Univ, Sch Life Sci, Technol Ctr Prot Sci, Minist Educ,Key Lab Prot Sci, Beijing, Peoples R China;

    Univ Calgary, Libin Cardiovasc Inst Alberta, Dept Physiol & Pharmacol, Calgary, AB, Canada;

    Tsinghua Univ, Sch Life Sci, Tsinghua Peking Joint Ctr Life Sci, Beijing Adv Innovat Ctr Struct Biol, Beijing, Peoples R China|Princeton Univ, Dept Mol Biol, Princeton, NJ 08540 USA;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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