Extracellular regulated kinase (ERK) 1/2 (MAPK1/3), P38 (MAPK14), c-Jun N-terminal kinase (JNK) (MAPK8), and ERK5 (MAPK7
) are four components of MAPK pathways. On activation, MAPKs phosphorylate and activate an array of transcription factors that regulate many important physiological and pathological processes in the cell including growth and differentiation, stress, adaptation to the environment, and the inflammatory response.,,,
However, down-regulated miR-143 significantly enhanced cell viability and the effect could be abrogated by ERK5 or MAPK7
miRNA Expression level Cellular process miR-181a Upregulated by morphine Promote astrocyte-preferential differentiation of NSPCs miR-23b Upregulated by morphine Adult neurogenesis miR-190 Downregulated by fentanyl Adult neurogenesis miR-143 Upregulation by IGF-1 Promotes proliferation, neural differentiation, and cell survival miR-181c Upregulation by IGF1/LIF Enhanced self-renewal of NSPCs miRNA Molecular target Reference miR-181a Prox1/Notch2  miR-23b Morphine receptor expression (MOR1)  miR-190 NeuroD  miR-143 PDGFRA, PRKCE, MAPK7
, DSSP, DMP-1,  KRAS, and BCL-2 miR-181c PTPN11, PTPN22, PTEN, Dusp6, PBX3, ZEB2,  and IRF8
As for MAPK7, such gene has been widely regarded as a multifunctional gene that involves various biological processes including proliferation, differentiation, transcription regulation, and development .
MAPK7 and MRAS are two proliferation-associated genes in our candidate epilepsy associated gene list.
Seven genes only (FOS, CDKN2D, MAP2K1, MAPK7, MAPK13, PDK1, and SFN) were characterised by an increase in their expression, whereas the expression of other genes was reduced.
We suppose that components of the MAPK- and PI3K/mTOR/PTEN-signalling cascades (FOS, MAPK7, MAPK13, MAP2K1, MTOR, PI3CA, PTEN, RHEB, RPS6KB1, and TP53) play an important role in cell motility [35, 36] and represent functional modules of this interactive network.