作者: Owen M Siggs , Carrie N Arnold , Christoph Huber , Elaine Pirie , Yu Xia
DOI: 10.1038/NI.2012
关键词:
摘要: B lymphopoiesis begins in the fetal liver, switching after birth to bone marrow, where it persists for life. The unique developmental outcomes of each phase are well documented, yet their molecular requirements not. Here we describe two allelic X-linked mutations mice that caused cell-intrinsic arrest adult lymphopoiesis. Mutant liver progenitors generated cells situ but not irradiated which emphasizes a necessity affected pathway only context marrow. causative were ascribed Atp11c, encodes P4-type ATPase with no previously described function. Our data establish an essential, cell-autonomous and context-sensitive function ATP11C, putative aminophospholipid flippase, cell development.