MAPK1
小结
MAPK1（也称为ERK2）是致癌基因，编码蛋白是丝氨酸/苏氨酸激酶，参与MAPK信号传导途径。其在促分裂原活化蛋白激酶（MAPK）信号级联中起效应蛋白的作用。MAPK信号传导途径参与多种细胞过程的调节，包括增殖，分化，细胞粘附和转录。作为三层MAPK级联的组分，ERK2活性依赖于上游MEK1 / 2激酶的磷酸化。活化的ERK2同源二聚体并磷酸化下游靶标，包括在细胞增殖和存活中具有中心作用的转录因子，例如RSK（核糖体S6激酶），MSK（促分裂原和应激激活的蛋白激酶）和MYC。然而，ERK2靶标还包括上游MAPK途径效应子，突出了ERK2在MAPK途径的负反馈中起作用。
MAPK1的突变和扩增在宫颈癌，头颈癌和卵巢癌中检测到。
MAPK1 (ERK2), a serine/threonine kinase, is altered by mutation or amplification in various cancer types including head and neck, cervical and ovarian cancer.MAPK1 (also known as ERK2) is a serine/threonine kinase that functions as an effector protein in the mitogen-activated protein kinase (MAPK) signaling cascade. The MAPK signaling pathway is involved in the regulation of diverse cellular processes including proliferation, differentiation, cell adhesion and transcription. As a component of a three-tiered MAPK cascade, ERK2 activity is dependent on phosphorylation by upstream MEK1/2 kinases. Activated ERK2 homodimerizes and phosphorylates downstream targets, including transcription factors with central roles in cell proliferation and survival such as RSK (ribosomal S6 kinase), MSK (mitogen- and stress-activated protein kinases) and MYC. However, ERK2 targets also include upstream MAPK pathway effectors, highlighting the role ERK2 plays in negative feedback on the MAPK pathway. ERK2 targets also include cytoskeletal molecules and nucleoporins. These signaling events are triggered by growth factors, cytokines and hormones that activate upstream receptor tyrosine kinases, ultimately leading to altered expression of key regulators of cell growth, differentiation, proliferation and survival. ERK2 and its homolog, ERK1 (MAPK3), are essential for cell proliferation; they are ubiquitously and often simultaneously expressed, but evidence suggests they may have some distinct functions in specialized contexts. ERK2 is infrequently mutated in human cancers; however, a recurrent ERK2 mutation is found in cervical and head and neck cancers and amplification is observed in ovarian cancer. Inhibitors of ERK1/2 are being explored as complementary and alternative options to RAF and MEK inhibition in cases of resistance or partial response.