Biphenotypic B-lymphoid/myeloid cells expressing low levels of Pax5: potential targets of BAL development.
Simmons, Szandor; Knoll, Marko; Drewell, Christopher; Wolf, Ingrid; Mollenkopf, Hans-Joachim; Bouquet, Corinne; Melchers, Fritz.
; 120(18): 3688-98, 2012 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-22927250
Single-cell trajectory detection uncovers progression and regulatory coordination in human B cell development.
Stage-specific control of early B cell development by the transcription factor Ikaros.
Mechanisms of clonal evolution in childhood acute lymphoblastic leukemia.
Superenhancer reprogramming drives a B-cell-epithelial transition and high-risk leukemia.
The transcription repressors Bach2 and Bach1 promote B cell development by repressing the myeloid program.
Loss of Ikaros DNA-binding function confers integrin-dependent survival on pre-B cells and progression to acute lymphoblastic leukemia.
Flexible ordering of antibody class switch and V(D)J joining during B-cell ontogeny.
Macrophage colony-stimulating factor receptor marks and regulates a fetal myeloid-primed B-cell progenitor in mice.
Pax5 loss imposes a reversible differentiation block in B-progenitor acute lymphoblastic leukemia.
The BTG2-PRMT1 module limits pre-B cell expansion by regulating the CDK4-Cyclin-D3 complex.