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Prepublished online as a Blood First Edition Paper on November 14, 2002; DOI 10.1182/blood-2002-07-2250.
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Blood, 15 March 2003, Vol. 101, No. 6, pp. 2250-2252
HEMATOPOIESIS
Brief report
Hematologic effects of inactivating the Ras processing enzyme
Rce1
Abigail L. Aiyagari,
Brigit
R. Taylor,
Vikas Aurora,
Stephen G. Young, and
Kevin M. Shannon
From the Departments of Pediatrics and
Medicine, Gladstone Institute of Cardiovascular Disease, and
Cardiovascular Research Institute, University of California, San
Francisco (UCSF), CA.
Posttranslational processing of Ras proteins has attracted
considerable interest as a potential target for anticancer drug discovery. Rce1 encodes an endoprotease that facilitates
membrane targeting of Ras and other prenylated proteins by releasing
the carboxyl-terminal 3 amino acids (ie, the -AAX of the CAAX
motif). Homozygous Rce1 mutant embryos
(Rce1 /) die late in gestation. To
characterize the role of Rce1 in hematopoiesis, we
performed adoptive transfers and investigated cells from the recipients. Rce1/ fetal liver cells rescued
lethally irradiated recipients and manifested normal long-term
repopulating potential in competitive repopulation assays. The
recipients of Rce1/ cells developed modest
elevations in mature myeloid cells (neutrophils + monocytes), but
remained well. Bone marrow cells from mice that received transplants
of Rce1/ activated extracellular
signal-related kinase (ERK) normally in response to
granulocyte-macrophage colony-stimulating factor. These data suggest
that pharmacologic inhibitors of Rce1 will have minimal effects on
normal hematopoietic cells.
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