(1) In short, Gene Ontology analysis has identified several potentially affected pathways involved in synaptic transmission (HTR2A, BDNF, CHRNA3, CHRNB4, DRD1, DRD2, DRD4, EGR1, GRIA4, GRIN2B, GRM3, NISCH, SLC1A3, and ERBB4
), dopamine metabolic processes (COMT, DRD1, DRD2, DRD4, MAOA, NR4A2, and SLC6A3), and ion channel activity (CHRNA7, CACNA1I, CACNB2, CHRNA3, CHRNA5, CHRNB4, GABRB3, GRIA4, GRIA1, GRIN2B, HCN1, CACNA1C, KCTD13, KCNV1, KCNN3, KCNJ13, and KCNB1).
EGFR (Epidermal growth factor receptor) belongs to the erbB family of closely related receptor tyrosine kinases, which include erbB1 (Also known as EGFR), erbB2 (HER2), erbB3, and erbB4
. Although their basic structures are similar, each one has distinct properties, including variation in tyrosine kinase activity.
The family of receptors in this group is made up of four homologous receptors: epidermal growth factor receptor (ErbB1/EGFR/HER1), HER2 (HER2/neu), ErbB3 (HER3) and ErbB4
Association between ErbB4
single nucleotide polymorphisms and susceptibility to schizophrenia: A meta-analysis of case-control studies.
Researchers showed mice lacking ErbB4
activity in specific brain regions performed poorly on timed attention tasks.
This gene family is composed of 4 members: HER1 (also known as EGFR), HER2, HER3 (also termed ERBB3), and HER4 (also termed ERBB4
Activated p38y MAPK Isoform Mediates Early Cardiogenesis Through NKx2.5 in Human Pluripotent Stem Cells," Stem Cells, vol.
NRG1 is an essential paracrine regulator of cell-cell communication through activation of ERBB4
, which further activates the PI3K/Akt pathway .
We found that, as compared to the other 1024 cancer cells, the overall EGFR expression in 12 thyroid cancer cells is significantly overexpressed with 1.7-folds (thyroid cancers versus other cancers = 7.302 [+ or -] 0.24 versus 6.53 [+ or -] 0.03 fluorescence intensity-[log.sup.2], P = 0.017), whereas the overall expressions of ERBB2, ERBB4
, and EGF show similar expressions in all cancer cells.
Canertinib is an irreversible inhibitor that binds covalently to specific cysteine residues in the ATP-binding pocket such as cysteine 773 of EGFR, cysteine 784 of ErbB2, and cysteine 778 of ErbB4
thereby blocking the ATP-binding site in the kinase domain of ErbB proteins, preventing their kinase activity and downstream signaling, and additionally, it also prevents transmodulation of ErbB2 .
This reduces miR-146 inhibition on its target gene ErbB4
and thus enhances signaling through the TGF-[beta]1-ErbB4 pathway, which increases autocrine synthesis of MCP-1, further reducing miR-146a levels  (Figure 1).
Wai et al., "ERBB4
confers metastatic capacity in Ewing sarcoma," EMBO Molecular Medicine, vol.