Marx S O, Reiken S, Hisamatsu Y, Gaburjakova M, Gaburjakova J, Yang Y M, Rosemblit N, Marks A R
Center for Molecular Cardiology, Department of Medicine, College of Physicians and Surgeons of Columbia University, 630 West 168th St., New York, NY 10032, USA.
J Cell Biol. 2001 May 14;153(4):699-708. doi: 10.1083/jcb.153.4.699.
Ryanodine receptors (RyRs), intracellular calcium release channels required for cardiac and skeletal muscle contraction, are macromolecular complexes that include kinases and phosphatases. Phosphorylation/dephosphorylation plays a key role in regulating the function of many ion channels, including RyRs. However, the mechanism by which kinases and phosphatases are targeted to ion channels is not well understood. We have identified a novel mechanism involved in the formation of ion channel macromolecular complexes: kinase and phosphatase targeting proteins binding to ion channels via leucine/isoleucine zipper (LZ) motifs. Activation of kinases and phosphatases bound to RyR2 via LZs regulates phosphorylation of the channel, and disruption of kinase binding via LZ motifs prevents phosphorylation of RyR2. Elucidation of this new role for LZs in ion channel macromolecular complexes now permits: (a) rapid mapping of kinase and phosphatase targeting protein binding sites on ion channels; (b) predicting which kinases and phosphatases are likely to regulate a given ion channel; (c) rapid identification of novel kinase and phosphatase targeting proteins; and (d) tools for dissecting the role of kinases and phosphatases as modulators of ion channel function.
兰尼碱受体(RyRs)是心肌和骨骼肌收缩所需的细胞内钙释放通道,是包含激酶和磷酸酶的大分子复合物。磷酸化/去磷酸化在调节包括RyRs在内的许多离子通道的功能中起关键作用。然而,激酶和磷酸酶靶向离子通道的机制尚未完全清楚。我们已经确定了一种参与离子通道大分子复合物形成的新机制:激酶和磷酸酶靶向蛋白通过亮氨酸/异亮氨酸拉链(LZ)基序与离子通道结合。通过LZs与RyR2结合的激酶和磷酸酶的激活调节通道的磷酸化,并且通过LZ基序破坏激酶结合可防止RyR2的磷酸化。阐明LZs在离子通道大分子复合物中的这一新作用现在允许:(a)快速绘制激酶和磷酸酶靶向蛋白在离子通道上的结合位点;(b)预测哪些激酶和磷酸酶可能调节给定的离子通道;(c)快速鉴定新的激酶和磷酸酶靶向蛋白;以及(d)用于剖析激酶和磷酸酶作为离子通道功能调节剂的作用的工具。