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Title: Tyrosine kinase activity of EphA2 promotes its S897 phosphorylation and glioblastoma cell proliferation
Authors: Hamaoka, Yuho
Negishi, Manabu  kyouindb  KAKEN_id
Katoh, Hironori  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0002-8191-8117 (unconfirmed)
Author's alias: 根岸, 学
加藤, 裕教
Keywords: EphA2
ERK
Cell proliferation
Glioblastoma
Issue Date: 23-May-2018
Publisher: Elsevier BV
Journal title: Biochemical and Biophysical Research Communications
Volume: 499
Issue: 4
Start page: 920
End page: 926
Abstract: EphA2, a member of the Eph family of receptor tyrosine kinases, has been reported to promote tumor malignancy through phosphorylation of serine 897 (S897). Here, we found that overexpression of wild-type EphA2 induced S897 phosphorylation through ERK activation without growth factors or cytokines and promoted glioblastoma cell proliferation. However, overexpression of a kinase-inactive mutant of EphA2 failed to induce ERK activation, S897 phosphorylation, and promotion of glioblastoma cell proliferation. These data suggest that when overexpressed, EphA2 induces ERK activation through its tyrosine kinase activity, leading to S897 phosphorylation and promotion of glioblastoma cell proliferation. Our findings provide a new insight into how EphA2 mediates glioblastoma progression.
Rights: © 2018. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/. The full-text file will be made open to the public on 23 May 2019 in accordance with publisher's 'Terms and Conditions for Self-Archiving'. This is not the published version. Please cite only the published version. この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。
URI: http://hdl.handle.net/2433/231897
DOI(Published Version): 10.1016/j.bbrc.2018.04.020
PubMed ID: 29626472
Appears in Collections:Journal Articles

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