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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

B-cell CLL/lymphoma 11A

BCL11A, Evi9, CTIP1
This gene encodes a C2H2 type zinc-finger protein by its similarity to the mouse Bcl11a/Evi9 protein. The corresponding mouse gene is a common site of retroviral integration in myeloid leukemia, and may function as a leukemia disease gene, in part, through its interaction with BCL6. During hematopoietic cell differentiation, this gene is down-regulated. It is possibly involved in lymphoma pathogenesis since translocations associated with B-cell malignancies also deregulates its expression. Multiple transcript variants encoding several different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: HBS1L, HAD, CAN, Beta-globin, EKLF
Papers on BCL11A
The genetic basis of asymptomatic codon 8 frame-shift (HBB:c25_26delAA) β(0) -thalassaemia homozygotes.
Chui et al., Boston, United States. In Br J Haematol, Feb 2016
On the three major HbF quantitative trait loci (QTL), the twins were homozygous for G>A HBG2 Xmn1 site at single nucleotide polymorphism (SNP) rs7482144, homozygous for 3-bp deletion HBS1L-MYB intergenic polymorphism (HMIP) at rs66650371, and heterozygous for the A>C BCL11A intron 2 polymorphism at rs766432.
Therapeutic fetal-globin inducers reduce transcriptional repression in hemoglobinopathy erythroid progenitors through distinct mechanisms.
Perrine et al., Boston, United States. In Blood Cells Mol Dis, Jan 2016
In studies here, representative molecules from four chemical classes, representing several distinct primary mechanisms of action, were investigated for effects on γ-globin transcriptional repressors, including components of the NuRD complex (LSD1 and HDACs 2-3), and the downstream repressor BCL11A, in erythroid progenitors from hemoglobinopathy patients.
Pomalidomide reverses γ-globin silencing through the transcriptional reprogramming of adult hematopoietic progenitors.
Blanc et al., United States. In Blood, Jan 2016
Further, the transcription networks involved in γ-globin repression were selectively and differentially affected by pomalidomide including BCL11A, SOX6, IKZF1, KLF1, and LSD1.
BCL11A expression in acute myeloid leukemia.
Yin et al., Suzhou, China. In Leuk Res, Jan 2016
BACKGROUND: BCL11A encodes a C2H2 type zinc-finger protein.
BCL11A enhancer dissection by Cas9-mediated in situ saturating mutagenesis.
Bauer et al., Boston, United States. In Nature, Dec 2015
Previously, we identified an erythroid enhancer of human BCL11A, subject to common genetic variation associated with the fetal haemoglobin level, the mouse orthologue of which is necessary for erythroid BCL11A expression.
A systematic review of known mechanisms of hydroxyurea-induced fetal hemoglobin for treatment of sickle cell disease.
Wonkam et al., Cape Town, South Africa. In Expert Rev Hematol, Oct 2015
RESULTS: Studies have provided consistent associations between genomic variations in HbF-promoting loci and variable HbF level in response to HU. Numerous signal transduction pathways have been implicated, through the identification of key genomic variants in BCL11A, HBS1L-MYB, SAR1 or XmnI polymorphism that predispose the response to the treatment, and signal transduction pathways that modulate γ-globin expression (cAMP/cGMP; Giα/c-Jun N-terminal kinase/Jun; methylation and miRNA).
Impact of epigenetic mechanisms on therapeutic approaches of hemoglobinopathies.
Napoli et al., Napoli, Italy. In Blood Cells Mol Dis, Aug 2015
Particularly interesting are the recent data on miRNAs showing the interaction of these molecules with different transcription factors such as MYB, KLF, BCL11A and SOX6.
Hemoglobin switching's surprise: the versatile transcription factor BCL11A is a master repressor of fetal hemoglobin.
Orkin et al., Boston, United States. In Curr Opin Genet Dev, Aug 2015
Recent genome-wide association studies implicated the zinc-finger transcriptional repressor BCL11A in fetal hemoglobin regulation.
Sickle cell disease and H3Africa: enhancing genomic research on cardiovascular diseases in African patients.
Members of the H3Africa Consortium et al., Cape Town, South Africa. In Cardiovasc J Afr, Mar 2015
Studies in Tanzania and Cameroon have reported that singlenucleotide polymorphisms in BCL11A and HBS1L-MYB loci and co-inheritance of alpha-thalassaemia impact on foetal haemoglobin levels and clinical severity.
The genomic and transcriptomic landscape of anaplastic thyroid cancer: implications for therapy.
Jones et al., Vancouver, Canada. In Bmc Cancer, 2014
RESULTS: The most prevalent mutations were those of TP53 and BRAF; repeated alterations of the epigenetic machinery such as frame-shift deletions of HDAC10 and EP300, loss of SMARCA2 and fusions of MECP2, BCL11A and SS18 were observed.
Fetal globin gene repressors as drug targets for molecular therapies to treat the β-globinopathies.
Engel et al., Sendai, Japan. In Mol Cell Biol, 2014
Multiple reports have now identified several transcription factors that are involved in fetal globin gene repression in definitive (adult)-stage erythroid cells (the TR2/TR4 heterodimer, MYB, KLFs, BCL11A, and SOX6).
An erythroid enhancer of BCL11A subject to genetic variation determines fetal hemoglobin level.
Orkin et al., Boston, United States. In Science, 2013
We found that common genetic variation at BCL11A associated with fetal hemoglobin (HbF) level lies in noncoding sequences decorated by an erythroid enhancer chromatin signature.
Proteomic and bioinformatic analysis of mammalian SWI/SNF complexes identifies extensive roles in human malignancy.
Crabtree et al., United States. In Nat Genet, 2013
To understand the full extent of their involvement, we conducted a proteomic analysis of endogenous mSWI/SNF complexes, which identified several new dedicated, stable subunits not found in yeast SWI/SNF complexes, including BCL7A, BCL7B and BCL7C, BCL11A and BCL11B, BRD9 and SS18.
Analysis of rs4671393 polymorphism in hemoglobin E/β-thalassemia major in Guangxi Province of China.
Luo et al., In J Pediatr Hematol Oncol, 2012
frequency of rs4671393(G->A) was relatively high in patients with HbE/[beta]-thalassemia of Guangxi province of China, accompanying with high level of HbF; polymorphism of rs4671393 possibly prevents severe complications in patients with HbE/[beta]-thalassemia
Single nucleotide polymorphisms in JAZF1 and BCL11A gene are nominally associated with type 2 diabetes in African-American families from the GENNID study.
American Diabetes Association GENNID Study Group et al., Winston-Salem, United States. In J Hum Genet, 2012
This study indicates a nominal role for JAZF1 and BCL11A variants in type 2 diabetes susceptibility in African-Americans.
The oncoprotein BCL11A binds to orphan nuclear receptor TLX and potentiates its transrepressive function.
Estébanez-Perpiñá et al., Barcelona, Spain. In Plos One, 2011
BCL11A is a novel TLX coregulator that might be involved in TLX-dependent gene regulation in the brain.
Correction of sickle cell disease in adult mice by interference with fetal hemoglobin silencing.
Orkin et al., Boston, United States. In Science, 2011
BCL11A is required for silencing of gamma-globin expression in adult animals yet dispensable for red cell production; inactivation of BCL11A in sickle cell disease (SCD) transgenic mice corrects defects associated with SCD through HbF induction
A functional element necessary for fetal hemoglobin silencing.
Bender et al., Boston, United States. In N Engl J Med, 2011
We found that a critical fetal hemoglobin silencing factor, BCL11A, and its partners bind within this region in the chromatin of adult erythroid cells.
Intramuscular administration of a VEGF zinc finger transcription factor activator (VEGF-ZFP-TF) improves functional outcomes in SOD1 rats.
Boulis et al., Atlanta, United States. In Amyotroph Lateral Scler, 2011
Administration of vascular endothelial growth factor (VEGF)-ZFP-TF may be neuroprotective and has potential as a safe and practical approach for management of motor disability in amyotrophic lateral sclerosis (ALS).
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