Institute for Research in Immunology and Cancer, Université de Montréal Montréal, QC, Canada.
Institute for Research in Immunology and Cancer, Université de MontréalMontréal, QC, Canada; Institute for Research in Cancer of MontpellierMontpellier, France.
Front Cell Dev Biol. 2016 Jun 27;4:67. doi: 10.3389/fcell.2016.00067. eCollection 2016.
The protein kinases ERK1 and ERK2 are the effector components of the prototypical ERK1/2 mitogen-activated protein (MAP) kinase pathway. This signaling pathway regulates cell proliferation, differentiation and survival, and is essential for embryonic development and cellular homeostasis. ERK1 and ERK2 homologs share similar biochemical properties but whether they exert specific physiological functions or act redundantly has been a matter of controversy. However, recent studies now provide compelling evidence in support of functionally redundant roles of ERK1 and ERK2 in embryonic development and physiology. In this review, we present a critical assessment of the evidence for the functional specificity or redundancy of MAP kinase isoforms. We focus on the ERK1/ERK2 pathway but also discuss the case of JNK and p38 isoforms.
蛋白激酶 ERK1 和 ERK2 是典型的 ERK1/2 丝裂原激活蛋白 (MAP) 激酶途径的效应成分。该信号通路调节细胞增殖、分化和存活，对胚胎发育和细胞内稳态至关重要。ERK1 和 ERK2 同源物具有相似的生化特性，但它们是否发挥特定的生理功能或冗余作用一直存在争议。然而，最近的研究现在提供了令人信服的证据，支持 ERK1 和 ERK2 在胚胎发育和生理中具有功能冗余的作用。在这篇综述中，我们对 MAP 激酶同工型的功能特异性或冗余性的证据进行了批判性评估。我们重点介绍了 ERK1/ERK2 途径，但也讨论了 JNK 和 p38 同工型的情况。
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