A truncated erythropoietin receptor that fails to prevent programmed cell death of erythroid cells.

Article Details

Citation

Nakamura Y, Komatsu N, Nakauchi H

A truncated erythropoietin receptor that fails to prevent programmed cell death of erythroid cells.

Science. 1992 Aug 21;257(5073):1138-41.

PubMed ID
1324524 [ View in PubMed
]
Abstract

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.

DrugBank Data that Cites this Article

Polypeptides
NameUniProt ID
Erythropoietin receptorP19235Details