A human B‐cell interactome identifies MYB and FOXM1 as master regulators of proliferation in germinal centers

Céline Lefèbvre(Columbia University), Presha Rajbhandari(Columbia University), Mariano J. Alvarez(Columbia University), Pradeep Bandaru(Columbia University), Wei Keat Lim(Columbia University), Mai Sato(Cancer Genetics (United States)), Kai Wang(Columbia University), Pavel Sumazin(Columbia University), Manjunath Kustagi(Columbia University), Brygida Bisikirska(Columbia University), Katia Basso(Cancer Genetics (United States)), Pedro Beltrão(University of California, San Francisco), Nevan J. Krogan(University of California, San Francisco), Jean Gautier(Cancer Genetics (United States)), Riccardo Dalla‐Favera(Cancer Genetics (United States)), Andrea Califano(Columbia University)
Molecular Systems Biology
June 8, 2010
Cited by 399Open Access
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Abstract

Assembly of a transcriptional and post-translational molecular interaction network in B cells, the human B-cell interactome (HBCI), reveals a hierarchical, transcriptional control module, where MYB and FOXM1 act as synergistic master regulators of proliferation in the germinal center (GC). Eighty percent of genes jointly regulated by these transcription factors are activated in the GC, including those encoding proteins in a complex regulating DNA pre-replication, replication, and mitosis. These results indicate that the HBCI analysis can be used for the identification of determinants of major human cell phenotypes and provides a paradigm of general applicability to normal and pathologic tissues.


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