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Necl-4 enhances the PLCγ-c-Raf-MEK-ERK pathway without affecting internalization of VEGFR2.
Yamana, Shota; Tokiyama, Amina; Fujita, Hidenobu; Terao, Yuya; Horibe, Sayo; Sasaki, Naoto; Satomi-Kobayashi, Seimi; Hirata, Ken-Ichi; Rikitake, Yoshiyuki.
Afiliação
  • Yamana S; Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Hyogo 650-0017, Japan.
  • Tokiyama A; Division of Signal Transduction, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe, Hyogo 650-0017, Japan.
  • Fujita H; Department of Medical Pharmaceutics, Kobe Pharmaceutical University, Kobe, Hyogo 658-8558, Japan.
  • Terao Y; Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Hyogo 650-0017, Japan; Department of Medical Pharmaceutics, Kobe Pharmaceutical University, Kobe, Hyogo 658-8558, Japan.
  • Horibe S; Department of Medical Pharmaceutics, Kobe Pharmaceutical University, Kobe, Hyogo 658-8558, Japan.
  • Sasaki N; Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Hyogo 650-0017, Japan; Department of Medical Pharmaceutics, Kobe Pharmaceutical University, Kobe, Hyogo 658-8558, Japan.
  • Satomi-Kobayashi S; Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Hyogo 650-0017, Japan.
  • Hirata KI; Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Hyogo 650-0017, Japan.
  • Rikitake Y; Division of Signal Transduction, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe, Hyogo 650-0017, Japan; Department of Medical Pharmaceutics, Kobe Pharmaceutical University, Kobe, Hyogo 658-8558, Japan. Electronic address: rikitake@kobepharma-u.ac.
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.
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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

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