首页> 美国卫生研究院文献>The Journal of Physiology >Rad and Rem are non‐canonical G‐proteins with respect to the regulatory role of guanine nucleotide binding in CaV1.2 channel regulation
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Rad and Rem are non‐canonical G‐proteins with respect to the regulatory role of guanine nucleotide binding in CaV1.2 channel regulation

机译:就鸟嘌呤核苷酸结合在CaV1.2通道调控中的调控作用而言Rad和Rem是非经典G蛋白

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摘要

Key points class="unordered" style="list-style-type:disc" id="tjp6876-list-0001">RGK (Rad, Rem, Rem2, Gem/Kir) proteins are small monomeric G‐proteins implicated in various cellular functions and disease states. All RGK proteins potently inhibit voltage‐gated calcium (CaV) channels.It is unclear whether RGK proteins are regulated by guanine nucleotide binding in a manner that conforms to a canonical G‐protein regulation paradigm.We utilized strategic Rad and Rem mutants together with a range of functional readouts (CaV1.2 currents, Ca2+ transients, CaVβ binding) in heterologous cells and cardiomyocytes to determine whether the function of these RGK proteins is regulated in a canonical manner.Our results demonstrate that Rad and Rem are non‐canonical G‐proteins with respect to the regulatory role of their guanine nucleotide binding domain in CaV1.2 channel regulation.Our findings offer deepened insights into cellular mechanisms governing RGK regulation and function, and contribute towards our understanding of their pathophysiological roles.
机译:关键点 class =“ unordered” style =“ list-style-type:disc” id =“ tjp6876-list-0001”> <!-list-behavior = unordered prefix-word = mark-type = disc max- label-size = 0-> liliRGK(Rad,Rem,Rem2,Gem / Kir)蛋白是小的单体G蛋白,涉及各种细胞功能和疾病状态。所有RGK蛋白均有效抑制电压门控钙(CaV)通道。 目前尚不清楚RGK蛋白是否受鸟嘌呤核苷酸结合调控的方式是否符合规范的G蛋白调控范式。 我们利用策略性Rad和Rem突变体以及异源细胞和心肌细胞中的一系列功能读数(CaV1.2电流,Ca 2 + 瞬变,CaVβ结合)来确定是否这些RGK蛋白以规范的方式调节。 我们的研究结果表明,就其鸟嘌呤核苷酸结合域在CaV1.2通道调节中的调节作用而言,Rad和Rem是非经典G蛋白。 我们的发现为控制RGK调节和功能的细胞机制提供了更深刻的见解,并有助于我们了解其病理生理作用。

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