Insulin-like growth factor (IGF) signaling requires αvβ3-IGF1- IGF type 1 receptor (IGF1R) ternary complex formation in anchorage independence, and the complex formation does not require IGF1R and Src activation

Masaaki Fujita, Yoko K. Takada, Yoshikazu Takada

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

Background: αvβ3 binds to IGF1, and the αvβ3-IGF1- IGF1R complex is formed in non-transformed cells. Results: IGF1 induces signals with the complex formation in anchorage independence. IGF1R or Src inhibitors did not suppress the complex formation. Conclusion: αvβ3-ECM interaction is not required for IGF signaling. The complex formation occurs before IGF1R activation. Significance: This study identifies new therapeutic targets in IGF signaling.

Original languageEnglish
Pages (from-to)3059-3069
Number of pages11
JournalJournal of Biological Chemistry
Volume288
Issue number5
DOIs
Publication statusPublished - Feb 1 2013
Externally publishedYes

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IGF Type 1 Receptor
Somatomedins
Chemical activation
Military electronic countermeasures
Therapeutics

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology

Cite this

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abstract = "Background: αvβ3 binds to IGF1, and the αvβ3-IGF1- IGF1R complex is formed in non-transformed cells. Results: IGF1 induces signals with the complex formation in anchorage independence. IGF1R or Src inhibitors did not suppress the complex formation. Conclusion: αvβ3-ECM interaction is not required for IGF signaling. The complex formation occurs before IGF1R activation. Significance: This study identifies new therapeutic targets in IGF signaling.",
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T1 - Insulin-like growth factor (IGF) signaling requires αvβ3-IGF1- IGF type 1 receptor (IGF1R) ternary complex formation in anchorage independence, and the complex formation does not require IGF1R and Src activation

AU - Fujita, Masaaki

AU - Takada, Yoko K.

AU - Takada, Yoshikazu

PY - 2013/2/1

Y1 - 2013/2/1

N2 - Background: αvβ3 binds to IGF1, and the αvβ3-IGF1- IGF1R complex is formed in non-transformed cells. Results: IGF1 induces signals with the complex formation in anchorage independence. IGF1R or Src inhibitors did not suppress the complex formation. Conclusion: αvβ3-ECM interaction is not required for IGF signaling. The complex formation occurs before IGF1R activation. Significance: This study identifies new therapeutic targets in IGF signaling.

AB - Background: αvβ3 binds to IGF1, and the αvβ3-IGF1- IGF1R complex is formed in non-transformed cells. Results: IGF1 induces signals with the complex formation in anchorage independence. IGF1R or Src inhibitors did not suppress the complex formation. Conclusion: αvβ3-ECM interaction is not required for IGF signaling. The complex formation occurs before IGF1R activation. Significance: This study identifies new therapeutic targets in IGF signaling.

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