Susan Winandy

TL;DR: It is proposed that Ikaros promotes differentiation of pluripotential hematopoietic stem cell(s) into the lymphocyte pathways through the erythroid and myeloid lineages in mutant mice.

TL;DR: The Ikaros gene family encodes zinc finger DNA-binding proteins essential for lineage determination and control of proliferation in the lymphoid system that are capable of targeting chromatin remodeling and deacetylation complexes in vivo, and it is proposed that the restructuring of chromatin is a key aspect of Ikaro function in lymphocyte differentiation.

TL;DR: It is proposed that within developing and mature T lymphocytes, distinct thresholds of Ikaros activity are required to regulate proliferation and that a decrease in Ikaro activity below the first threshold causes the rapid accumulation of T lymphoblasts, whereas a further decrease leads to neoplastic transformation.

TL;DR: A model is proposed that defines Ikaros as the backbone of a complex regulatory protein network that controls cell fate decisions and regulates homeostasis in the hemo-lymphoid system.

TL;DR: It is shown that the transcription factor EBF restored the generation of CD19+ pro–B cells from Ikaros-deficient hematopoietic progenitors, and is an obligate component of a network that regulates B cell fate commitment and immunoglobulin heavy-chain gene recombination.