Necl-4 enhances the PLCγ-c-Raf-MEK-ERK pathway without affecting internalization of VEGFR2.
Biochem Biophys Res Commun
; 490(2): 169-175, 2017 08 19.
Article
em En
| MEDLINE
| ID: mdl-28601637
We have reported that knockdown of Necl-4 decreases vascular endothelial growth factor (VEGF)-induced phosphorylation of extracellular signal-regulated kinase (ERK) without affecting phosphorylation of VEGF receptor 2 (VEGFR2) in sparsely cultured human umbilical vein endothelial cells (HUVECs). However, the underlying molecular mechanism is unknown. Compared with control HUVECs, VEGF-induced phosphorylation of phospholipase Cγ (PLCγ), c-Raf, mitogen-activated protein kinase/ERK kinase (MEK) and ERK were all inhibited in Necl-4-knockdown HUVECs. However, VEGF-induced internalization of VEGFR2 was not different between control and Necl-4-knockdown HUVECs. We have reported that protein-tyrosine phosphatase, non-receptor type 13 (PTPN13) and Rho-associated kinase (ROCK) are involved in the Necl-4-knockdown-induced inhibition of the VEGF-induced activation of Rac1. However, the effects of Necl-4-knockdown on VEGF-induced phosphorylation of VEGFR2 and ERK were not affected either by knockdown of PTPN13 or by ROCK inhibitors. These results suggest that Necl-4 enhances VEGF-induced activation of PLCγ-c-Raf-MEK-ERK pathway without affecting the phosphorylation and internalization of VEGFR2.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Imunoglobulinas
/
Moléculas de Adesão Celular
/
Proteínas Proto-Oncogênicas c-raf
/
Proteínas Quinases Ativadas por Mitógeno
/
Receptor 2 de Fatores de Crescimento do Endotélio Vascular
/
MAP Quinases Reguladas por Sinal Extracelular
/
Fosfolipase C gama
Limite:
Humans
Idioma:
En
Ano de publicação:
2017
Tipo de documento:
Article