Abstract:
:G-CSF-induced myeloid differentiation of 32Dcl3 murine myeloblast cells is antagonized by concurrent exposure to interleukin-3 (IL-3) or by oncogenic transformation of 32Dcl3 by src- or abl-oncogenes which render the cells IL-3-independent. Recent reports have linked G-CSF-mediated differentiation to the ability of G-CSF to activate Stat3. We hypothesized that IL-3 suppresses 32Dcl3 differentiation in part through disruption of G-CSF-Stat signalling. We report that IL-3 inhibited the ability of G-CSF to induce Stat3 DNA binding. Moreover, we find that G-CSF activation of Stat3 binding to DNA is biphasic, peaking at 15-30 min and again at 6-8 h; both peaks are inhibited by IL-3. Transformation of 32Dcl3 cells by the v-abl oncogene leads to constitutive Stat3 activation and distinctive Stat-DNA-binding patterns which are not affected by G-CSF. Cross-modulation of Stat pathway signalling could be a physiologic mechanism for establishing a hierarchy of growth factor effects upon a cell exposed at once to multiple cytokines.
journal_name
Leukemiajournal_title
Leukemiaauthors
Steinman RA,Iro Adoi
10.1038/sj.leu.2401253subject
Has Abstractpub_date
1999-01-01 00:00:00pages
54-61issue
1eissn
0887-6924issn
1476-5551journal_volume
13pub_type
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