Notch1 perturbation of hemopoiesis involves non-cell-autonomous modifications

Journal of Immunology

Volumn 168, Issue 4, 2002, Pages 1738-1745

  Kawamata, Shin ^a   Du, Changchun ^a   Li, Kaijun ^a   Lavau, Catherine ^a  

^a SAINT LOUIS HOSPITAL   (France)

Author keywords

[No Author keywords available]

Indexed keywords

NOTCH RECEPTOR; NOTCH1 RECEPTOR; UNCLASSIFIED DRUG;

ANIMAL CELL; ARTICLE; B LYMPHOCYTE; BONE MARROW CELL; BONE MARROW TRANSPLANTATION; CELL CULTURE; CELL DIFFERENTIATION; CELL LINEAGE; CELL MATURATION; CONTROLLED STUDY; HEMATOPOIESIS; MOUSE; NONHUMAN; PRIORITY JOURNAL; T CELL LEUKEMIA; T CELL LYMPHOMA; T LYMPHOCYTE;

EID: 0037083598     PISSN: 00221767     EISSN: None     Source Type: Journal    
DOI: 10.4049/jimmunol.168.4.1738     Document Type: Article

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5. Constitutively active human Notch1 binds to the transcription factor CBF1 and stimulates transcription through a promoter containing a CBF1-responsive element
6. δ-1 activation of notch-1 signaling results in HES-1 transactivation
7. Hes1 and Hes5 as notch effectors in mammalian neuronal differentiation
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9. Notch inhibition of E47 supports the existence of a novel signaling pathway
10. Fringe, a boundary-specific signaling molecule, mediates interactions between dorsal and ventral cells during Drosophila wing development
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12. Fringe boundaries coincide with Notch-dependent patterning centres in mammals and alter Notch-dependent development in Drosophila
13. Limb morphogenesis: Connections between patterning and growth
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21. Notch 1-deficient common lymphoid precursors adopt a β cell fate in the thymus
22. Subversion of the T/B lineage decision in the thymus by lunatic fringe-mediated inhibition of Notch-1
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25. Inhibition of granulocytic differentiation by mNotch1
26. Overexpression of wild-type retinoic acid receptor α (RARα) recapitulates retinoic acid-sensitive transformation of primary myeloid progenitors by acute promyelocytic leukemia RARα-fusion genes
27. Versatile retroviral vectors for potential use in gene therapy
28. The oncogenic capacity of HRX-ENL requires the transcriptional transactivation activity of ENL and the DNA binding motifs of HRX
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