Dr. Xu received his Bachelor’s degree from Fudan University in 2000 and PhD from UCLA in 2008. His Ph.D. dissertation in Dr. Stephen Smale’s lab focused on transcriptional regulatory processes during early mammalian development. Currently, he is an HHMI-Helen Hay Whitney Fellow in Dr. Stuart Orkin’s laboratory at Children’s Hospital Boston, Harvard Medical School. Dr. Xu’s primary area of investigation is developmental gene regulation with a focus on genetic and epigenetic control of hematopoietic genes during normal and pathological conditions.

The title of his recent Science paper is “Correction of Sickle Cell Disease in Adult Mice by Interference with Fetal Hemoglobin Silencing” [Science. 2011 Oct 13. Epub ahead of print]. Here is the short description of his work:

Persistence of human fetal hemoglobin in adults lessens the severity of sickle cell disease (SCD) and the beta-thalassemias. Here we show that the transcription factor BCL11A is required in vivo for silencing of gamma-globin expression in adult animals, yet dispensable for red cell production. BCL11A serves as a barrier to HbF reactivation by known HbF inducing agents. In a proof-of-principle test of BCL11A as a potential therapeutic target, we demonstrate that inactivation of BCL11A in SCD transgenic mice corrects the hematologic and pathologic defects associated with SCD through high-level pancellular HbF induction. Thus, interference with HbF silencing by manipulation of a single target protein is sufficient to reverse SCD.

If anyone is interested in his research, you can email him directly at xu@bloodgroup.tch.harvard.edu