作者: Emmanuelle Passegué , Erwin F Wagner , Irving L Weissman , None
DOI: 10.1016/J.CELL.2004.10.010
关键词: Transcriptional regulation 、 Transcription factor 、 Myelopoiesis 、 Haematopoiesis 、 JUNB 、 Stem cell 、 Immunology 、 Cancer research 、 Chronic myelogenous leukemia 、 Progenitor cell 、 Biology
摘要: The AP-1 transcription factor JunB is a transcriptional regulator of myelopoiesis. Inactivation in postnatal mice results myeloproliferative disorder (MPD) resembling early human chronic myelogenous leukemia (CML). Here, we show that regulates the numbers hematopoietic stem cells (HSC). overexpression decreases frequency long-term HSC (LT-HSC), while inactivation specifically expands LT-HSC and granulocyte/macrophage progenitors (GMP) resulting MPD. Further, demonstrate junB must take place LT-HSC, not at later stages myelopoiesis, to induce MPD only junB-deficient are capable transplanting recipient mice. These cell-specific role for normal leukemic hematopoiesis provide experimental evidence (LSC) can reside stage development mouse model