Abstract:
:The c-Myb transcription factor is crucial during definitive hematopoiesis. However, the embryonic lethality of Myb traditional null mutations has precluded analysis of c-Myb function in lymphocytes. Using tissue-specific inactivation at the Myb locus, we demonstrate that loss of Myb causes a partial block during B cell development at the pro-B to pre-B cell transition, resulting in greatly decreased output of new B cells from the bone marrow. Furthermore, we demonstrate that Myb is not essential for the proliferation of splenic B cells, but that loss of c-Myb function prevents normal B cell homeostasis due to decreased splenic B cell survival. Decreased survival is accompanied by hyporesponsiveness to the B cell survival factor BLyS (also termed BAFF), decreased expression of the BLyS receptor 3 (BR3), and altered regulation of PKCdelta nuclear accumulation. Thus, c-Myb is important during multiple stages of B-lymphopoiesis.
journal_name
Immunityjournal_title
Immunityauthors
Thomas MD,Kremer CS,Ravichandran KS,Rajewsky K,Bender TPdoi
10.1016/j.immuni.2005.08.005keywords:
subject
Has Abstractpub_date
2005-09-01 00:00:00pages
275-86issue
3eissn
1074-7613issn
1097-4180pii
S1074-7613(05)00244-Xjournal_volume
23pub_type
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