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Updated: May 3, 2026

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
09:29

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies

Published on: September 30, 2016

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ネトリン-1媒介のアクソン外成長は,大腸がん依存のMAPK活性化で削除される必要があります

Christelle Forcet1, Elke Stein, Laurent Pays

  • 1Apoptosis/Differentiation Laboratory label 'La Ligue' Molecular and Cellular Genetic Center, CNRS UMR 5534, University of Lyon, 69622 Villeurbanne, France.

Nature
|May 3, 2002
PubMed
まとめ

ネトリン-1は,大腸がん (Dcc) のデリテッド受容体 (Dcc) 経由で開発中の軸索を誘導する. この研究では,Dccがミトゲン活性化タンパク質キナーゼ (MAPK) 信号伝達を活性化することが明らかになり,これは軸索の成長と誘導に不可欠です.

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