Dendritic cell fate is determined by BCL11A. - Wikidata - awgldk - TriplyDB

Dendritic cell fate is determined by BCL11A.

Dendritic cell fate is determined by BCL11A.

http://www.wikidata.org/entity/Q37659927

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Investigating Evolutionary Conservation of Dendritic Cell Subset Identity and Functions BCL11A deletions result in fetal hemoglobin persistence and neurodevelopmental alterations.Hemoglobin switching's surprise: the versatile transcription factor BCL11A is a master repressor of fetal hemoglobin.Defining Mononuclear Phagocyte Subset Homology Across Several Distant Warm-Blooded Vertebrates Through Comparative Transcriptomics.A Druggable TCF4- and BRD4-Dependent Transcriptional Network Sustains Malignancy in Blastic Plasmacytoid Dendritic Cell Neoplasm.Subtype-specific addiction of the activated B-cell subset of diffuse large B-cell lymphoma to FOXP1.Genetic treatment of a molecular disorder: gene therapy approaches to sickle cell disease.The multifaceted biology of plasmacytoid dendritic cells.miRNA-embedded shRNAs for Lineage-specific BCL11A Knockdown and Hemoglobin F Induction Transcriptional Control of Dendritic Cell Development.Plasmacytoid dendritic cells: development, functions, and role in atherosclerotic inflammation.Forging T-Lymphocyte Identity: Intersecting Networks of Transcriptional Control.Dendritic cell analysis in primary immunodeficiency Isoform-Specific Expression and Feedback Regulation of E Protein TCF4 Control Dendritic Cell Lineage Specification.Gene expression profiling of Mycobacterium tuberculosis Lipoarabinomannan-treated macrophages: A role of the Bcl-2 family member A1 in inhibition of apoptosis in mycobacteria-infected macrophages.Bcl11a Deficiency Leads to Hematopoietic Stem Cell Defects with an Aging-like Phenotype.Strict in vivo specificity of the Bcl11a erythroid enhancer.Recent progress in understanding and manipulating haemoglobin switching for the haemoglobinopathies.A Nonhuman Primate Transplantation Model to Evaluate Hematopoietic Stem Cell Gene Editing Strategies for β-Hemoglobinopathies.Corrected and Republished from: BCL11A Is a Critical Component of a Transcriptional Network That Activates RAG Expression and V(D)J Recombination.Direct Promoter Repression by BCL11A Controls the Fetal to Adult Hemoglobin Switch.Molecular regulation of dendritic cell development and function in homeostasis, inflammation, and cancer.Discovering human diabetes-risk gene function with genetics and physiological assays

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Dendritic cell fate is determined by BCL11A.

http://www.wikidata.org/entity/Q37659927

description

article científic

@ca

article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 03 March 2014

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Dendritic cell fate is determined by BCL11A.

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Dendritic cell fate is determined by BCL11A.

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type

label

Dendritic cell fate is determined by BCL11A.

@en

Dendritic cell fate is determined by BCL11A.

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prefLabel

Dendritic cell fate is determined by BCL11A.

@en

Dendritic cell fate is determined by BCL11A.

@nl

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PNAS.1319228111

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Proceedings of the National Academy of Sciences of the United States of America

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Dendritic cell fate is determined by BCL11A.

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Arthur L Shaffer

http://www.w3.org/2001/XMLSchema#string

Baeck-Seung Lee

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Bum-Kyu Lee

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Gregory C Ippolito

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Haley O Tucker

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Jason K Wall

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Jian Lin

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Joseph D Dekker

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Louis M Staudt

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Vishwanath R Iyer

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P2860

Functional studies of BCL11A: characterization of the conserved BCL11A-XL splice variant and its interaction with BCL6 in nuclear paraspeckles of germinal center B cells

E2A basic-helix-loop-helix transcription factors are negatively regulated by serum growth factors and by the Id3 protein

Id helix-loop-helix proteins antagonize pax transcription factor activity by inhibiting DNA binding

A gene atlas of the mouse and human protein-encoding transcriptomes

Transcription factor E2-2 is an essential and specific regulator of plasmacytoid dendritic cell development

Lymphoid-specific expression of the Id3 gene in hematopoietic cells. Selective antagonism of E2A basic helix-loop-helix protein associated with Id3-induced differentiation of erythroleukemia cells

Development of human plasmacytoid dendritic cells depends on the combined action of the basic helix-loop-helix factor E2-2 and the Ets factor Spi-B

Developmental and species-divergent globin switching are driven by BCL11A

A genomic regulatory element that directs assembly and function of immune-specific AP-1-IRF complexes

Bcl11a is essential for normal lymphoid development

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E998-1006

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scholarly article

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10.1073/PNAS.1319228111

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111

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2014-03-03T00:00:00Z

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