Pseudoenzymes are emerging as significant mediators and regulators of signal transduction. These proteins maintain enzyme folds and topologies, but are disrupted in the conserved motifs required for enzymatic activity. Among the pseudoenzymes, the pseudoGTPase group of atypical GTPases has recently expanded and includes the Rnd and RGK groups, RhoH and the RhoBTB proteins, mitochondrial RhoGTPase and centaurin‐γ groups, CENP‐M, dynein LIC, Entamoeba histolytica RabX3, leucine‐rich repeat kinase 2, and the p190RhoGAP proteins. The wide range of cellular functions associated with pseudoGTPases includes cell migration and adhesion, membrane trafficking and cargo transport, mitosis, mitochondrial activity, transcriptional control, and autophagy, placing the group in an expanding portfolio of signaling pathways. In this review, we examine how the pseudoGTPases differ from canonical GTPases and consider their mechanistic and functional roles in signal transduction. We review the amino acid differences between the pseudoGTPases and discuss how these proteins can be classified based on their ability to bind nucleotide and their enzymatic activity. We discuss the molecular and structural consequences of amino acid divergence from canonical GTPases and use comparison with the well‐studied pseudokinases to illustrate the classifications. PseudoGTPases are fast becoming recognized as important mechanistic components in a range of cellular roles, and we provide a concise discussion of the currently identified members of this group.

中文翻译：

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假酶的假GTPase 组。

假酶正在成为信号转导的重要介质和调节剂。这些蛋白质维持酶的折叠和拓扑结构，但酶活性所需的保守基序被破坏。在假酶中，非典型 GTP 酶的假 GTP 酶组最近已扩展，包括 Rnd 和 RGK 组、RhoH 和 RhoBTB 蛋白、线粒体 RhoGTPase 和半人马蛋白-γ 组、CENP-M、动力蛋白 LIC、溶组织内阿米巴RabX3、富含亮氨酸重复序列激酶 2 和 p190RhoGAP 蛋白。与伪 GTP 酶相关的广泛细胞功能包括细胞迁移和粘附、膜运输和货物运输、有丝分裂、线粒体活性、转录控制和自噬，使该组处于不断扩大的信号通路组合中。在这篇综述中，我们研究了伪 GTP 酶与典型 GTP 酶的不同之处，并考虑了它们在信号转导中的机制和功能作用。我们回顾了假 GTP 酶之间的氨基酸差异，并讨论了如何根据这些蛋白质结合核苷酸的能力及其酶活性对它们进行分类。我们讨论了经典 GTP 酶氨基酸差异的分子和结构后果，并通过与经过充分研究的假激酶进行比较来说明分类。伪 GTP 酶很快被认为是一系列细胞作用中的重要机制组成部分，我们对当前确定的该组成员进行了简要讨论。