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Blood, 1 May 2002, Vol. 99, No. 9, pp. 3213-3219
HEMATOPOIESIS
Accumulation of c-Cbl and rapid termination of colony-stimulating
factor 1 receptor signaling in interferon consensus sequence binding
protein-deficient bone marrow-derived macrophages
Axel Kallies,
Frank Rosenbauer,
Marina Scheller,
Klaus-Peter Knobeloch, and
Ivan Horak
From the Department of Molecular Genetics, Institute of
Molecular Pharmacology, and Medical Center Benjamin Franklin, Free
University of Berlin, Germany.
Mice deficient for the transcription factor interferon consensus
sequence binding protein (ICSBP) are immunodeficient and develop
granulocytic leukemia. Further analyses indicated that ICSBP is a
molecular switch factor directing the differentiation of bipotential
myeloid precursors to the monocytic lineage. To reveal the molecular
mechanisms responsible for the deregulation of myelopoiesis, we
examined the signaling of the colony-stimulating factor 1 receptor
(CSF-1R) in bone marrow-derived macrophages (BMMs) from
ICSBP / mice. We found that in the absence of ICSBP,
CSF-1R signaling is attenuated as seen from an accelerated termination
of Erk phosphorylation and reduced cell growth. This finding coincides
with an increased CSF-1R ubiquitination and an enhanced accumulation of
c-Cbl. c-Cbl is an ubiquitin-ligase known to down-regulate activated
CSF-1R by targeting it to the endocytic pathway. Our results indicate that upon CSF-1R activation, c-Cbl itself is partly proteolytically degraded in ICSBP+/+ but not in ICSBP/
BMMs. Congruently, the expression of a major
endosomal/lysosomal protease, cathepsin B, is strongly
reduced in ICSBP/ BMMs.
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