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Science 21 August 1992:
Vol. 257. no. 5073, pp. 1138 - 1141
DOI: 10.1126/science.257.5073.1138
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Articles

A Truncated Erythropoietin Receptor That Fails to Prevent Programmed Cell Death of Erythroid Cells

Yukio Nakamura 1, Norio Komatsu 1, and Hiromitsu Nakauchi 1

1 Laboratory of Cell Growth and Differentiation, Tsukuba Life Science Center, The Institute of Physical and Chemical Research (RIKEN), 3-1-1, Koyadai, Tsukuba, Japan

A form of the human erythropoietin receptor (EPOR) was identified in which the cytoplasmic region is truncated by alternative splicing. The truncated form of the receptor (EPOR-T) is the most prevalent form of EPOR in early-stage erythroid progenitor cells, but the full-length EPOR (EPOR-F) becomes the most prevalent form in late-stage progenitors. EPOR-T can transduce a mitogenic signal. However, cells transfected with EPOR-T are more prone to programmed cell death than those expressing EPOR-F. EPOR-F may transduce a signal to prevent programmed cell death that is independent of the mitogenic signal, and alternative splicing of the EPOR gene may have an important role in erythropoiesis.


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