Longwood Scientific Salon: Hemoglobin switching and sickle cell disease, by Dr. Xu Jian

Dec - 06
2011

Longwood Scientific Salon: Hemoglobin switching and sickle cell disease, by Dr. Xu Jian

Dear CSSA members,

Dr.Jian Xu will be giving a seminar in the Longwood Scientific Salon (LSS) about the “Hemoglobin switching and sickle cell disease”, which has been published in Science recently, on Dec. 6th, Tuesday.

Dr. Xu obtained his Ph.D. from UCLA, and now a postdoc fellow in Dr. Stuart Orkin’s laboratory, Harvard Medical School, Children’s hospital & Howard Hughes Medical Institute.

Dr. Xu has achieved remarkably during his postdoc career and in graduate school. He had published many first-author papers in Nature, Science and Genes & Development, et al. He has also been awarded for many awards and grants, including NIH K01 grant, the Helen Hay Whitney Foundation-HHMI Post-Doctoral Fellowship and American Society of Hematology Merit Award, which are all extremely competitive and hard to get.

Please join us to meet Dr. Jian Xu, learn about his outstanding research and experience, as well as share great science! We are looking forward to seeing you there!

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LSS Cancer/Stem cell group event:

Speaker: Dr. Jian Xu
Time: 5:30pm-6:30pm, Dec. 6th, Tuesday
Location: Dana Farber Cancer Institute, Yawkey Center Room 308
(Yawkey is the big glass building at the corner of jimmy fund way and brookline avenue,
connecting with smith building)
Organizer: HMS-CSSA

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Title: Hemoglobin switching and sickle cell disease

Dr. Jian Xu

Abstract
Persistence of human fetal hemoglobin (HbF) in adults lessens the severity of sickle cell disease (SCD) and the beta-thalassemias. Here we show that the repressor BCL11A is required in vivo for silencing of fetal hemoglobin 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.