Sfpi1/PU.1 mutations in mouse radiation-induced acute myeloid leukaemias affect mRNA and protein abundance and associate with disrupted transcription

Natalie Brown, Rosemary Finnon, Robert Bulman, Paul Finnon, J. Moody, Simon Bouffler, Christophe Badie*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)

Abstract

Radiation-induced acute myeloid leukaemias (AMLs) in mice are characterised by deletions and point mutations in the Sfpi1/PU.1 transcription factor. Six AML cell lines were used to examine the impact of three previously described R235 point mutations. AML cells carry myeloid and stem cell markers and the R235 mutations differentially affect mRNA and protein abundance. Expression of Sfpi1/PU.1 target genes was deregulated in a broadly similar fashion irrespective of R235 mutation including Flt3, which is frequently subject to activating mutations in human myeloid leukaemias. While R235 mutations differentially affect protein abundance they resulted in similar disruption of Sfpi1/PU.1 functions.

Original languageEnglish
Pages (from-to)126-132
Number of pages7
JournalLeukemia Research
Volume35
Issue number1
DOIs
Publication statusPublished - Jan 2011

Bibliographical note

Funding Information:
The authors would like to thank Dr. Kazuko Yoshida (NIRS, Chiba, Japan) for the gift of 8016, 8709 and 7926 cell lines, Dr. Andrew Riches (University of St. Andrews, UK) for SA2, and Drs. Emmy Meijne and Rene Huiskamp (NRG, Petten, Netherlands) for MLP3 and 3124. This work was supported by US Department of Energy grant DE-FG02-05ER63947 .

Keywords

  • Mutation
  • Myeloid leukaemia
  • Phosphorylation
  • Radiation
  • Sfpi1/PU.1
  • Transcription

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