Point mutation in the exoplasmic domain of the erythropoietin receptor resulting in hormone-independent activation and tumorigenicity

Akihiko Yoshimura, Gregory Longmore, Harvey F. Lodish

研究成果: Article査読

251 被引用数 (Scopus)

抄録

THE receptors for erythropoietin and other cytokines constitute a new superfamily1-4. They have no tyrosine-kinase or other enzyme motif and their signal-transducing mechanism is unclear. Here we describe two classes of activating mutations in the erythropoietin receptor (EPOR). A single point mutation in the exoplasmic domain enables it to induce hormone-independent cell growth and tumorigenesis after expression in nontumorigenic, interleukin-3-dependent haematopoietic cells. A C-terminal truncation in the cytoplasmic domain of the EPOR renders the receptor hyper-responsive to erythropoietin, but is insufficient to induce hormone-independent growth or tumorigenicity. The activating point mutation retards intracellular transport and turnover of the receptor. These alterations in metabolism and tumorigenicity caused by the EPOR with activating point mutations are similar to those observed in erythropoietin-independent activation of the wild type EPOR by association with gp55, the Friend spleen focus-forming virus glycoprotein5,6.

本文言語English
ページ(範囲)647-649
ページ数3
ジャーナルNature
348
6302
DOI
出版ステータスPublished - 1990
外部発表はい

ASJC Scopus subject areas

  • 一般

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