論文

査読有り 国際誌
2014年

Altered trafficking of mutated growth factor receptors and their associated molecules: implication for human cancers.

Cellular logistics
  • Shunsuke Kon
  • ,
  • Nobuhide Kobayashi
  • ,
  • Masanobu Satake

4
開始ページ
e28461
終了ページ
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.4161/cl.28461

Ligand-stimulated receptor tyrosine kinases (RTKs) are phosphorylated/ubiquitinated, endocytosed and transported to the lysosomes via endosomes/multivesicular bodies, resulting in the attenuation of signal transmission. If this physiological mechanism of RTK signal downregulation is perturbed, signal transduction persists and may contribute to cellular transformation. This article presents several such examples. In some cases, endocytosis is impaired, and the activated RTK remains on the plasma membrane. In other cases, the activated RTK is endocytosed into endosomes/multivesicular bodies, but not subsequently sorted to the lysosomes for degradation. The latter cases indicate that even endocytosed RTKs can transmit signals. Transport of RTKs is accomplished via the formation and movement of membrane vesicles. Blockage or delay of endocytosis/trafficking can be caused by genetic alterations in the RTK itself or by mutations in CBL, Arf GAPs, or other components involved in internalization and vesicle transport. A survey of the literature indicates that, in some cases, even RTKs synthesized de novo can initiate signaling at the endoplasmic reticulum/Golgi before reaching the plasma membrane. The spectrum of molecules targeted by the signal is likely to be different between cell surface- and endoplasmic reticulum/Golgi-localized RTKs.

リンク情報
DOI
https://doi.org/10.4161/cl.28461
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/25210647
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4156482
ID情報
  • DOI : 10.4161/cl.28461
  • ISSN : 2159-2780
  • PubMed ID : 25210647
  • PubMed Central 記事ID : PMC4156482

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