Architecture of a lymphomyeloid developmental switch controlled by PU.1, Notch and Gata3.
about
Transcriptional network control of normal and leukaemic haematopoiesisTranscriptional establishment of cell-type identity: dynamics and causal mechanisms of T-cell lineage commitment.Asynchronous combinatorial action of four regulatory factors activates Bcl11b for T cell commitmentBcl11b and combinatorial resolution of cell fate in the T-cell gene regulatory network.T cell development requires constraint of the myeloid regulator C/EBP-α by the Notch target and transcriptional repressor Hes1.GATA-3 dose-dependent checkpoints in early T cell commitment.A unifying gene signature for adenoid cystic cancer identifies parallel MYB-dependent and MYB-independent therapeutic targets.Regulation of early T-lineage gene expression and developmental progression by the progenitor cell transcription factor PU.1.Irreversibility of T-Cell Specification: Insights from Computational Modelling of a Minimal Network Architecture.Transcription Factor Bcl11b Controls Identity and Function of Mature Type 2 Innate Lymphoid Cells.Positive feedback between PU.1 and the cell cycle controls myeloid differentiationTranscriptional control of early T and B cell developmental choicesDevelopmental gene networks: a triathlon on the course to T cell identity.Forging T-Lymphocyte Identity: Intersecting Networks of Transcriptional Control.Transcription factors and target genes of pre-TCR signaling.The RUNX1-PU.1 axis in the control of hematopoiesis.Hematopoiesis and T-cell specification as a model developmental system.Cytokines, Transcription Factors, and the Initiation of T-Cell Development.The Regulatory Capacity of Bivalent Genes-A Theoretical Approach.Chemokine polyreactivity of IL7Rα+CSF-1R+ lympho-myeloid progenitors in the developing fetal liverTranscriptional regulation of IL-15 expression during hematopoiesis.Fitting structure to function in gene regulatory networks.Asynchronous lineage priming determines commitment to T cell and B cell lineages in fetal liver.Recurrent SPI1 (PU.1) fusions in high-risk pediatric T cell acute lymphoblastic leukemia.Delta-like 4-mediated Notch signaling is required for early T-cell development in a three-dimensional thymic structure.Pioneering, chromatin remodeling, and epigenetic constraint in early T-cell gene regulation by SPI1 (PU.1)Transcription Factor PU.1 Represses and Activates Gene Expression in Early T Cells by Redirecting Partner Transcription Factor Binding
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P2860
Architecture of a lymphomyeloid developmental switch controlled by PU.1, Notch and Gata3.
description
2013 nî lūn-bûn
@nan
2013年の論文
@ja
2013年論文
@yue
2013年論文
@zh-hant
2013年論文
@zh-hk
2013年論文
@zh-mo
2013年論文
@zh-tw
2013年论文
@wuu
2013年论文
@zh
2013年论文
@zh-cn
name
Architecture of a lymphomyeloid developmental switch controlled by PU.1, Notch and Gata3.
@ast
Architecture of a lymphomyeloid developmental switch controlled by PU.1, Notch and Gata3.
@en
type
label
Architecture of a lymphomyeloid developmental switch controlled by PU.1, Notch and Gata3.
@ast
Architecture of a lymphomyeloid developmental switch controlled by PU.1, Notch and Gata3.
@en
prefLabel
Architecture of a lymphomyeloid developmental switch controlled by PU.1, Notch and Gata3.
@ast
Architecture of a lymphomyeloid developmental switch controlled by PU.1, Notch and Gata3.
@en
P2860
P356
P1433
P1476
Architecture of a lymphomyeloid developmental switch controlled by PU.1, Notch and Gata3.
@en
P2093
Marissa Morales Del Real
P2860
P304
P356
10.1242/DEV.088559
P407
P577
2013-03-01T00:00:00Z