Expression of notch receptors, notch ligands, and fringe genes in hematopoiesis

Singh, Nidhi; Phillips, Robert A.; Iscove, Norman N.; Egan, Sean E.

doi:10.1016/s0301-472x(00)00146-6

Cited by 102 publications

(68 citation statements)

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“…Mast cells express specific pattern of Notch family members, low level of Notch-1, high level of Notch-2 and detectable level of Notch-3 (42). Mast cells also express Jagged-1 (43). It is well-known that GATA-3 and Notch are indispensable for T cell development, because deficiency of either of them blocks T cell development at earliest progenitor stage (35,44).…”

Section: Notch and Myeloid Cell Differentiationmentioning

confidence: 99%

Notch signaling in differentiation and function of dendritic cells

Cheng

Gabrilovich

2007

Immunol Res

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Hematopoietic stem cells give rise to multiple lineages of cells. This process is governed by a tightly controlled signaling network regulated by cytokines and a direct cell-cell. Notch signaling represents one of the major pathways activated during direct interaction between hematopoietic progenitor cells and bone marrow stroma. A critical role of Notch signaling in differentiation of T and B lymphocytes has now been established. Until recently, the role of Notch signaling in the development of myeloid cells and particular dendritic cells remained unclear. In this review we discuss recent exciting findings that shed light on the critical role of Notch in differentiation and the function of dendritic cells and its impact on immune responses.

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Section: Notch and Myeloid Cell Differentiationmentioning

confidence: 99%

Notch signaling in differentiation and function of dendritic cells

Cheng

Gabrilovich

2007

Immunol Res

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“…2 Notch signaling elements are expressed during embryonic and adult hematopoiesis. [9][10][11] During embryogenesis, hematopoiesis takes place in two different sites, the yolk sac (YS) and the para-aortic splanchnopleura region (P-Sp). [12][13][14] Primitive hematopoiesis begins in the mouse at E7.0-7.5 in the YS blood islands as a transient wave that involves the production of primitive nucleated erythrocytes and certain myeloid progenitor cells.…”

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confidence: 99%

Notch1 regulates progenitor cell proliferation and differentiation during mouse yolk sac hematopoiesis

et al. 2014

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Loss-of-function studies have demonstrated the essential role of Notch in definitive embryonic mouse hematopoiesis. We report here the consequences of Notch gain-of-function in mouse embryo hematopoiesis, achieved by constitutive expression of Notch1 intracellular domain (N1ICD) in angiopoietin receptor tyrosine kinase receptor-2 (Tie2)-derived enhanced green fluorescence protein (EGFP þ ) hematovascular progenitors. At E9.5, N1ICD expression led to the absence of the dorsal aorta hematopoietic clusters and of definitive hematopoiesis. The EGFP þ transient multipotent progenitors, purified from E9.5 to 10.5 Tie2-Cre;N1ICD yolk sac (YS) cells, had strongly reduced hematopoietic potential, whereas they had increased numbers of hemogenic endothelial cells. Late erythroid cell differentiation stages and mature myeloid cells (Gr1 þ , MPO þ ) were also strongly decreased. In contrast, EGFP þ erythro-myeloid progenitors, immature and intermediate differentiation stages of YS erythroid and myeloid cell lineages, were expanded. Tie2-Cre;N1ICD YS had reduced numbers of CD41 þ þ megakaryocytes, and these produced reduced below-normal numbers of immature colonies in vitro and their terminal differentiation was blocked. Cells from Tie2-Cre;N1ICD YS had a higher proliferation rate and lower apoptosis than wild-type (WT) YS cells. Quantitative gene expression analysis of FACS-purified EGFP þ YS progenitors revealed upregulation of Notch1-related genes and alterations in genes involved in hematopoietic differentiation. These results represent the first in vivo evidence of a role for Notch signaling in YS transient definitive hematopoiesis. Our results show that constitutive Notch1 activation in Tie2 þ cells hampers YS hematopoiesis of E9.5 embryos and demonstrate that Notch signaling regulates this process by balancing the proliferation and differentiation dynamics of lineage-restricted intermediate progenitors.

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“…Despite the fact that Notch1 signaling has a very specific function in the differentiation of CLPs, Notch1, 2, 3 and their ligands are expressed widely in the bone marrow (BM) and during T cell differentiation (13)(14)(15). Signals through the Notch receptors are regulated by multiple mechanisms.…”

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confidence: 99%

Notch-Regulated Ankyrin-Repeat Protein Inhibits Notch1 Signaling: Multiple Notch1 Signaling Pathways Involved In T Cell Development

Yun¹,

Bevan

2003

The Journal of Immunology

112

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We have characterized the function of Notch-regulated ankyrin-repeat protein (Nrarp) in mouse cell lines and in hematopoietic stem cells (HSCs). Nrarp overexpression is able to block Notch-induced activation of CBF-1. In AKR1010 thymoma cells, Nrarp overexpression blocks CBF-1-dependent transcriptional activation of Notch-responsive genes and inhibits phenotypic changes associated with Notch activation. Enforced expression of Nrarp in mouse HSCs results in a profound block in T lineage commitment and progression through early stages of thymocyte maturation. In contrast, Deltex-1 overexpression in HSCs can also block T lineage commitment but not progression through the early double negative stages of thymocyte maturation. The different effects of Deltex-1 and Nrarp overexpression suggest that alternate Notch signaling pathways mediate T vs B lineage commitment and thymocyte maturation.

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Expression of notch receptors, notch ligands, and fringe genes in hematopoiesis

Cited by 102 publications

References 100 publications

Notch signaling in differentiation and function of dendritic cells

Notch signaling in differentiation and function of dendritic cells

Notch1 regulates progenitor cell proliferation and differentiation during mouse yolk sac hematopoiesis

Notch-Regulated Ankyrin-Repeat Protein Inhibits Notch1 Signaling: Multiple Notch1 Signaling Pathways Involved In T Cell Development

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