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Article: Alternative promoter usage at the Notch1 locus supports ligand-independent signaling in T cell development and leukemogenesis

TitleAlternative promoter usage at the Notch1 locus supports ligand-independent signaling in T cell development and leukemogenesis
Authors
Issue Date2010
PublisherCell Press. The Journal's web site is located at http://www.elsevier.com/locate/immuni
Citation
Immunity, 2010, v. 33 n. 5, p. 685-698 How to Cite?
AbstractLoss of the transcription factor Ikaros is correlated with Notch receptor activation in T cell acute lymphoblastic leukemia (T-ALL). However, the mechanism remains unknown. We identified promoters in Notch1 that drove the expression of Notch1 proteins in the absence of a ligand. Ikaros bound to both canonical and alternative Notch1 promoters and its loss increased permissive chromatin, facilitating recruitment of transcription regulators. At early stages of leukemogenesis, increased basal expression from the canonical and 5'-alternative promoters initiated a feedback loop, augmenting Notch1 signaling. Ikaros also repressed intragenic promoters for ligand-independent Notch1 proteins that are cryptic in wild-type cells, poised in preleukemic cells, and active in leukemic cells. Only ligand-independent Notch1 isoforms were required for Ikaros-mediated leukemogenesis. Notch1 alternative-promoter usage was observed during T cell development and T-ALL progression. Thus, a network of epigenetic and transcriptional regulators controls conventional and unconventional Notch signaling during normal development and leukemogenesis. © 2010 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/180744
ISSN
2015 Impact Factor: 24.082
2015 SCImago Journal Rankings: 16.215
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorGómezDel Arco, Pen_US
dc.contributor.authorKashiwagi, Men_US
dc.contributor.authorJackson, AFen_US
dc.contributor.authorNaito, Ten_US
dc.contributor.authorZhang, Jen_US
dc.contributor.authorLiu, Fen_US
dc.contributor.authorKee, Ben_US
dc.contributor.authorVooijs, Men_US
dc.contributor.authorRadtke, Fen_US
dc.contributor.authorRedondo, JMen_US
dc.contributor.authorGeorgopoulos, Ken_US
dc.date.accessioned2013-01-28T01:42:11Z-
dc.date.available2013-01-28T01:42:11Z-
dc.date.issued2010en_US
dc.identifier.citationImmunity, 2010, v. 33 n. 5, p. 685-698en_US
dc.identifier.issn1074-7613en_US
dc.identifier.urihttp://hdl.handle.net/10722/180744-
dc.description.abstractLoss of the transcription factor Ikaros is correlated with Notch receptor activation in T cell acute lymphoblastic leukemia (T-ALL). However, the mechanism remains unknown. We identified promoters in Notch1 that drove the expression of Notch1 proteins in the absence of a ligand. Ikaros bound to both canonical and alternative Notch1 promoters and its loss increased permissive chromatin, facilitating recruitment of transcription regulators. At early stages of leukemogenesis, increased basal expression from the canonical and 5'-alternative promoters initiated a feedback loop, augmenting Notch1 signaling. Ikaros also repressed intragenic promoters for ligand-independent Notch1 proteins that are cryptic in wild-type cells, poised in preleukemic cells, and active in leukemic cells. Only ligand-independent Notch1 isoforms were required for Ikaros-mediated leukemogenesis. Notch1 alternative-promoter usage was observed during T cell development and T-ALL progression. Thus, a network of epigenetic and transcriptional regulators controls conventional and unconventional Notch signaling during normal development and leukemogenesis. © 2010 Elsevier Inc.en_US
dc.languageengen_US
dc.publisherCell Press. The Journal's web site is located at http://www.elsevier.com/locate/immunien_US
dc.relation.ispartofImmunityen_US
dc.subject.meshAnimalsen_US
dc.subject.meshEpigenomicsen_US
dc.subject.meshGene Expression Regulation, Leukemicen_US
dc.subject.meshGenetic Locien_US
dc.subject.meshIkaros Transcription Factor - Genetics - Metabolismen_US
dc.subject.meshLymphocyte Activation - Geneticsen_US
dc.subject.meshMiceen_US
dc.subject.meshPrecursor T-Cell Lymphoblastic Leukemia-Lymphoma - Geneticsen_US
dc.subject.meshPromoter Regions, Geneticen_US
dc.subject.meshReceptor, Notch1 - Genetics - Metabolismen_US
dc.subject.meshSignal Transduction - Geneticsen_US
dc.subject.meshT-Lymphocytes - Metabolismen_US
dc.titleAlternative promoter usage at the Notch1 locus supports ligand-independent signaling in T cell development and leukemogenesisen_US
dc.typeArticleen_US
dc.identifier.emailZhang, J: jzhang1@hku.hken_US
dc.identifier.authorityZhang, J=rp01713en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.immuni.2010.11.008en_US
dc.identifier.pmid21093322-
dc.identifier.scopuseid_2-s2.0-78650213618en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78650213618&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume33en_US
dc.identifier.issue5en_US
dc.identifier.spage685en_US
dc.identifier.epage698en_US
dc.identifier.isiWOS:000286082600008-
dc.publisher.placeUnited Statesen_US
dc.identifier.f10006641956-
dc.identifier.scopusauthoridGómezdel Arco, P=6506180533en_US
dc.identifier.scopusauthoridKashiwagi, M=36892980600en_US
dc.identifier.scopusauthoridJackson, AF=7402785468en_US
dc.identifier.scopusauthoridNaito, T=7202253732en_US
dc.identifier.scopusauthoridZhang, J=22137260600en_US
dc.identifier.scopusauthoridLiu, F=36067802500en_US
dc.identifier.scopusauthoridKee, B=7004240910en_US
dc.identifier.scopusauthoridVooijs, M=6602835614en_US
dc.identifier.scopusauthoridRadtke, F=7003909967en_US
dc.identifier.scopusauthoridRedondo, JM=7005458058en_US
dc.identifier.scopusauthoridGeorgopoulos, K=7006021598en_US

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