@article{cf8f0c9e9f0847dd99c13495d20be459,
title = "Bcl11a is essential for normal lymphoid development",
abstract = "Bcl11a (also called Evi9) functions as a myeloid or B cell proto-oncogene in mice and humans, respectively. Here we show that Bcl11a is essential for postnatal development and normal lymphopoiesis. Bcl11a mutant embryos lack B cells and have alterations in several types of T cells. Phenotypic and expression studies show that Bcl11 a functions upstream of the transcription factors Ebf1 and Pax5 in the B cell pathway. Transplantation studies show that these defects in Bcl11a mutant mice are intrinsic to fetal liver precursor cells. Mice transplanted with Bcl11a-deficient cells died from T cell leukemia derived from the host. Thus, Bcl11a may also function as a non-autonomous T cell tumor suppressor gene.",
author = "Pentao Liu and Keller, {Jonathan R.} and Mariaestela Ortiz and Lino Tessarollo and Rachel, {Rivka A.} and Takuro Nakamura and Jenkins, {Nancy A.} and Copeland, {Neal G.}",
note = "Funding Information: We thank S. Spence and T. Kuwata for reviewing the manuscript; D. Swing for help with mouse breeding; J. Wine for tail vein injection; K. Noer and R. Matthai for help with flow cytometry; and the Publication Department of NCI Frederick for graphic illustration. This work was supported by the NCI, Department of Health and Human Services (P.L., N.A.J., N.G.C.). This publication has been funded in whole or in part with federal funds from the NCI, NIH, under contract number NO1-CO-12400 (J.R.K., M.O.). The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does the mention of trade names, commercial products or organizations imply endorsement by the US Government.",
year = "2003",
month = jun,
day = "1",
doi = "10.1038/ni925",
language = "English (US)",
volume = "4",
pages = "525--532",
journal = "Nature immunology",
issn = "1529-2908",
publisher = "Nature Publishing Group",
number = "6",
}