MAPK6和MAPK4(又称ERK3和ERK4)是脊椎动物特有的非典型MAP激酶。非典型MAPK的特征不如传统MAPK，一般根据其缺乏MAPKK家族成员的激活而归类为非典型MAPK。与传统的MAPK蛋白不同，MAPK6和mapk4有一个单一的Ser-Glu-Gly磷酸化受体基序(库伦和Meloche, 2007;Cargnello et al, 2011)。MAPK6的独特之处还在于它是一种不稳定的激酶，其周转是由泛素依赖性降解介导的(Coulombe等，2003;库仑等，2004)。MAPK6和mapk4的生物学功能和调控途径尚不明确。MAPK6和4以RAC或cdc42依赖的方式在I类p21激活激酶(PAKs)下游磷酸化(Deleris et al, 2008;Perander等人，2008;Deleris等，2011; De La Mota-Peynado et al, 2011). One of the only well established substrates of MAPK6 and 4 is MAPKAPK5, which contributes to cell motility by promoting the HSBP1-dependent rearrangement of F-actin (Gerits et al, 2007; Kostenko et al, 2009a; reviewed in Kostenko et al, 2011b). The atypical MAPKs also contribute to cell motility and invasiveness through the NCOA3:ETV4-dependent regulation of MMP gene expression (Long et al, 2012; Yan et al, 2008; Qin et al, 2008). Both of these pathways may be misregulated in human cancers (reviewed in Myant and Sansom, 2011; Kostenko et al, 2012)
