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Schroeder, T. ; Just, U.

mNotch1 signaling reduces proliferation of myeloid progenitor cells by altering cell-cycle kinetics.

Exp. Hematol. 28, 1206-1213 (2000)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Objective. Notch receptors are involved in the regulation of cell-fate decisions, differentiation, and proliferation in many tissues. The expression of Notch receptors on hemopoietic cells and of cognate ligands on bone marrow stromal cells suggests a possible role for Notch signaling in the regulation of hemopoiesis, me were interested to assess the involvement of Notch1 signaling on cell proliferation of myeloid progenitor cells, Materials and Methods. Proliferation, cell-cycle status, and apoptosis of myeloid progenitor 32D cell lines engineered to permit the conditional induction of the constitutively active intracellular domain of mNotch1 (mN1(IC)) by the 4-hydroxytamoxifen(OHT)-inducible system were analyzed in the presence or absence of OHT. Results. The induction of mN1(IC) by OHT resulted in reduction of proliferation (p < 0.01) and accumulation of cells in the G(1)/G(0) phase of the cell cycle (p < 0.001) without substantially affecting apoptosis of 32D cells, These effects were observed under culture conditions that allow differentiation and, to a lesser degree, under conditions that normally promote self-renewal in the absence of differentiated cells. Conclusion. Our data suggest that mNotch1 signaling suppresses proliferation of myeloid progenitor cells by altering cell-cycle kinetics.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter cell proliferation; cell cycle; Notch1; 32D cell line; DROSOPHILA NOTCH; HUMAN HOMOLOG; MOUSE NOTCH; GRANULOCYTIC DIFFERENTIATION; INTRACELLULAR DOMAIN; FATE DETERMINATION; ANKYRIN REPEATS; C-ELEGANS; EXPRESSION; GENE
ISSN (print) / ISBN 0301-472X
e-ISSN 0301-472X
Zeitschrift Experimental Hematology
Quellenangaben Band: 28, Heft: 11, Seiten: 1206-1213 Artikelnummer: , Supplement: ,
Verlag Elsevier
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Clinical Molecular Biology and Tumor Genetics (K.MOLBI)