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http://purl.uniprot.org/citations/21189289http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21189289http://www.w3.org/2000/01/rdf-schema#comment"Early thymocytes possess multilineage potential, which is progressively restricted as cells transit through the double-negative stages of T-cell development. DN1 cells retain the ability to become natural killer cells, dendritic cells, B cells, and myeloid cells as well as T cells, but these options are lost by the DN3 stage. The Notch1 signaling pathway is indispensable for initiation of the T-cell lineage and inhibitory for the B-cell lineage, but the regulatory mechanisms by which the T-cell fate is locked in are largely undefined. Previously, we discovered that the E-protein transcription factor HEBAlt promoted T-cell specification. Here, we report that HEB(-/-) T-cell precursors have compromised Notch1 function and lose T-cell potential. Moreover, reconstituting HEB(-/-) precursors with Notch1 activity enforced fidelity to the T-cell fate. However, instead of becoming B cells, HEB(-/-) DN3 cells adopted a DN1-like phenotype and could be induced to differentiate into thymic NK cells. HEB(-/-) DN1-like cells retained GATA3 and Id2 expression but had lower levels of the Bcl11b gene, a Notch target gene. Therefore, our studies have revealed a new set of interactions between HEB, Notch1, and GATA3 that regulate the T-cell fate choice in developing thymocytes."xsd:string
http://purl.uniprot.org/citations/21189289http://purl.org/dc/terms/identifier"doi:10.1128/mcb.01034-10"xsd:string
http://purl.uniprot.org/citations/21189289http://purl.uniprot.org/core/author"Braunstein M."xsd:string
http://purl.uniprot.org/citations/21189289http://purl.uniprot.org/core/author"Anderson M.K."xsd:string
http://purl.uniprot.org/citations/21189289http://purl.uniprot.org/core/date"2011"xsd:gYear
http://purl.uniprot.org/citations/21189289http://purl.uniprot.org/core/name"Mol Cell Biol"xsd:string
http://purl.uniprot.org/citations/21189289http://purl.uniprot.org/core/pages"971-982"xsd:string
http://purl.uniprot.org/citations/21189289http://purl.uniprot.org/core/title"HEB-deficient T-cell precursors lose T-cell potential and adopt an alternative pathway of differentiation."xsd:string
http://purl.uniprot.org/citations/21189289http://purl.uniprot.org/core/volume"31"xsd:string
http://purl.uniprot.org/citations/21189289http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/21189289
http://purl.uniprot.org/citations/21189289http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/21189289
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http://purl.uniprot.org/uniprot/#_P23772-mappedCitation-21189289http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21189289
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http://purl.uniprot.org/uniprot/#_Q3UXQ3-mappedCitation-21189289http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21189289
http://purl.uniprot.org/uniprot/#_Q3TZD6-mappedCitation-21189289http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21189289
http://purl.uniprot.org/uniprot/#_Q3UZ69-mappedCitation-21189289http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21189289
http://purl.uniprot.org/uniprot/#_Q3UZA4-mappedCitation-21189289http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21189289
http://purl.uniprot.org/uniprot/#_Q01705-mappedCitation-21189289http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21189289
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http://purl.uniprot.org/uniprot/#_Q8BY39-mappedCitation-21189289http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21189289
http://purl.uniprot.org/uniprot/#_Q3TE72-mappedCitation-21189289http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21189289