The regulation of the phosphorylation of mitogen‐activated protein kinases (MAPKs) is essential for cellular processes such as proliferation, differentiation, survival, and death. Mutations within the MAPK signaling cascades are implicated in diseases such as cancer, neurodegenerative disorders, arthritis, obesity, and diabetes. MAPK phosphorylation is controlled by an intricate balance between MAPK kinases (enzymes that add phosphate groups) and MAPK phosphatases (MKPs) (enzymes that remove phosphate groups). MKPs are complex negative regulators of the MAPK pathway that control the amplitude and spatiotemporal regulation of MAPKs. MK‐STYX (MAPK phosphoserine/threonine/tyrosine‐binding protein) is a member of the MKP subfamily, which lacks the critical histidine and nucleophilic cysteine residues in the active site required for catalysis. MK‐STYX does not influence the phosphorylation status of MAPK, but even so it adds to the complexity of signal transduction cascades as a signaling regulator. This review highlights the function of MK‐STYX, providing insight into MK‐STYX as a signal regulating molecule in the stress response, HDAC 6 dynamics, apoptosis, and neurite differentiation.

中文翻译：

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伪磷酸酶MK-STYX：MAP激酶磷酸酶的非典型成员。

丝裂原激活的蛋白激酶（MAPK）磷酸化的调节对于细胞的增殖，分化，存活和死亡等细胞过程至关重要。MAPK信号级联内的突变与诸如癌症，神经退行性疾病，关节炎，肥胖症和糖尿病等疾病有关。MAPK磷酸化由MAPK激酶（添加磷酸基团的酶）和MAPK磷酸酶（MKPs）（除去磷酸基团的酶）之间的复杂平衡控制。MKP是MAPK通路的复杂负调节剂，它控制MAPK的振幅和时空调节。MK-STYX（MAPK磷酸丝氨酸/苏氨酸/酪氨酸结合蛋白）是MKP亚家族的成员，该亚家族在催化所需的活性位点缺少关键的组氨酸和亲核半胱氨酸残基。MK‐STYX不会影响MAPK的磷酸化状态，但即使如此，它也会增加信号转导级联作为信号调节剂的复杂性。这篇综述重点介绍了MK‐STYX的功能，深入了解了MK‐STYX作为应激反应，HDAC 6动力学，细胞凋亡和神经突分化中的信号调节分子。