Transcriptional silencing of -globin by BCL11A involves long-range interactions and cooperation with SOX6
نویسندگان
چکیده
منابع مشابه
Transcriptional silencing of {gamma}-globin by BCL11A involves long-range interactions and cooperation with SOX6.
The developmental switch from human fetal (gamma) to adult (beta) hemoglobin represents a clinically important example of developmental gene regulation. The transcription factor BCL11A is a central mediator of gamma-globin silencing and hemoglobin switching. Here we determine chromatin occupancy of BCL11A at the human beta-globin locus and other genomic regions in vivo by high-resolution chroma...
متن کاملTranscriptional silencing of -globin by BCL11A involves long-range interactions and cooperation with SOX6
Article is available under a Creative Commons license; see publisher's site for details. The MIT Faculty has made this article openly available. Please share how this access benefits you. Your story matters.
متن کاملTranscriptional regulators Myb and BCL11A interplay with DNA methyltransferase 1 in developmental silencing of embryonic and fetal β-like globin genes.
The clinical symptoms of hemoglobin disorders such as β-thalassemia and sickle cell anemia are significantly ameliorated by the persistent expression of γ-globin after birth. This knowledge has driven the discovery of important regulators that silence γ-globin postnatally. Improved understanding of the γ- to β-globin switching mechanism holds the key to devising targeted therapies for β-hemoglo...
متن کاملCorepressor-dependent silencing of fetal hemoglobin expression by BCL11A.
Reactivation of fetal hemoglobin (HbF) in adults ameliorates the severity of the common β-globin disorders. The transcription factor BCL11A is a critical modulator of hemoglobin switching and HbF silencing, yet the molecular mechanism through which BCL11A coordinates the developmental switch is incompletely understood. Particularly, the identities of BCL11A cooperating protein complexes and the...
متن کاملErythropoiesis and globin switching in compound Klf1::Bcl11a mutant mice.
B-cell lymphoma 11A (BCL11A) downregulation in human primary adult erythroid progenitors results in elevated expression of fetal γ-globin. Recent reports showed that BCL11A expression is activated by KLF1, leading to γ-globin repression. To study regulation of erythropoiesis and globin expression by KLF1 and BCL11A in an in vivo model, we used mice carrying a human β-globin locus transgene with...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Genes & Development
سال: 2010
ISSN: 0890-9369
DOI: 10.1101/gad.1897310