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  Deficiency of the adaptor SLP-65 in pre-B-cell acute lymphoblastic leukaemia

Jumaa, H., Bossaller, L., Portugal, K., Storch, B., Lotz, M., Flemming, A., et al. (2003). Deficiency of the adaptor SLP-65 in pre-B-cell acute lymphoblastic leukaemia. Nature, 423(6938), 452-456.

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Jumaa, Hassan1, Autor           
Bossaller, Lukas1, Autor           
Portugal, Karina1, Autor           
Storch, Bettina1, Autor           
Lotz, Michael1, Autor           
Flemming, Alexandra1, Autor           
Schrappe, Martin, Autor
Postila, Ville, Autor
Riikonen, Pekka, Autor
Pelkonen, Jukka, Autor
Niemeyer, Charlotte M., Autor
Reth, Michael1, Autor           
Affiliations:
1Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243645              

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 Zusammenfassung: Acute lymphoblastic leukaemia (ALL) is the commonest form of childhood malignancy, and most cases arise from B-cell clones arrested at the pre-B-cell stage of differentiation1,2. The molecular events that arrest pre-B-cell differentiation in the leukaemic pre-B cells have not been well characterized. Here we show that the differentiation regulator SLP-65 (an adaptor protein also called BLNK or BASH3-6) inhibits pre-B-cell leukaemia in mice. Reconstitution of SLP-65 expression in a SLP-65-/- pre-B-cell line led to enhanced differentiation in vitro and prevented the development of pre-B-cell leukaemia in immune-deficient mice. Tyrosine 96 of SLP-65 was required for this activity. The murine SLP-65-/- pre-B-cell leukaemia resembles human childhood pre-B ALL. Indeed, 16 of the 34 childhood pre-B ALL samples that were tested showed a complete loss or drastic reduction of SLP-65 expression. This loss is probably due to the incorporation of alternative exons into SLP-65 transcripts, leading to premature stop codons. Thus, the somatic loss of SLP-65 and the accompanying block in pre-B-cell differentiation might be one of the primary causes of childhood pre-B ALL.

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Sprache(n): eng - English
 Datum: 2003-05-22
 Publikationsstatus: Erschienen
 Seiten: -
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: -
 Identifikatoren: eDoc: 126299
ISI: 000183012000045
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Titel: Nature
  Alternativer Titel : Nature
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: -
Seiten: - Band / Heft: 423 (6938) Artikelnummer: - Start- / Endseite: 452 - 456 Identifikator: ISSN: 0028-0836