Recruitment of the nuclear receptor corepressor N-CoR by the TEL moiety of the childhood leukemia-associated TEL-AML1 oncoprotein

F. Guidez, Petrie Kevin Petrie, A. M. Ford, H. Lu, C. A. Bennett, A. MacGregor, J. Hannemann, Y. Ito, J. Ghysdael, M. Greaves, L. M. Wiedemann, Arthur Z Zelent

Research output: Contribution to journalArticle

96 Citations (Scopus)

Abstract

The t(12;21)(p13;q22) chromosomal translocation is the most frequent illegitimate gene recombination in a pediatric cancer and occurs in approximately 25% of common acute lymphoblastic leukemia (cALL) cases. This rearrangement results in the in frame fusion of the 5'-region of the ETS-related gene, TEL (ETV6), to almost the entire acute myeloid leukemia 1 (AML 1)(also called CBFA2 or PEBP2AB1) locus and expression of the TEL-AML1 chimeric protein. Although AML1 stimulates transcription, TEL-AML1 functions as a repressor of some AML1 target genes. In contrast to the wild type AML1 protein, both TEL and TEL-AML1 interact with N-CoR, a component of the nuclear receptor compressor complex with histone deacetylase activity. The interaction between TEL and N-CoR requires the central region of TEL, which is retained in TEL-AML1, and TEL lacking this domain is impaired in transcriptional repression. Taken together, our results suggest that TEL-AML1 may contribute to leukemogenesis by recruiting N-CoR to AML1 target genes and thus imposing an altered pattern of their expression. (C) 2000 by the American Society of Hematology.

Original languageEnglish (US)
Pages (from-to)2557-2561
Number of pages5
JournalBlood
Volume96
Issue number7
StatePublished - Oct 1 2000
Externally publishedYes

Fingerprint

Co-Repressor Proteins
Oncogene Proteins
Leukemia
Genes
Genetic Translocation
Pediatrics
Histone Deacetylases
Transcription
Cytoplasmic and Nuclear Receptors
Precursor Cell Lymphoblastic Leukemia-Lymphoma
Acute Myeloid Leukemia
Genetic Recombination
Compressors
Fusion reactions
Neoplasms
Proteins
TEL-AML1 fusion protein

ASJC Scopus subject areas

  • Hematology
  • Biochemistry
  • Cell Biology
  • Immunology

Cite this

Guidez, F., Kevin Petrie, P., Ford, A. M., Lu, H., Bennett, C. A., MacGregor, A., ... Zelent, A. Z. (2000). Recruitment of the nuclear receptor corepressor N-CoR by the TEL moiety of the childhood leukemia-associated TEL-AML1 oncoprotein. Blood, 96(7), 2557-2561.

Recruitment of the nuclear receptor corepressor N-CoR by the TEL moiety of the childhood leukemia-associated TEL-AML1 oncoprotein. / Guidez, F.; Kevin Petrie, Petrie; Ford, A. M.; Lu, H.; Bennett, C. A.; MacGregor, A.; Hannemann, J.; Ito, Y.; Ghysdael, J.; Greaves, M.; Wiedemann, L. M.; Zelent, Arthur Z.

In: Blood, Vol. 96, No. 7, 01.10.2000, p. 2557-2561.

Research output: Contribution to journalArticle

Guidez, F, Kevin Petrie, P, Ford, AM, Lu, H, Bennett, CA, MacGregor, A, Hannemann, J, Ito, Y, Ghysdael, J, Greaves, M, Wiedemann, LM & Zelent, AZ 2000, 'Recruitment of the nuclear receptor corepressor N-CoR by the TEL moiety of the childhood leukemia-associated TEL-AML1 oncoprotein', Blood, vol. 96, no. 7, pp. 2557-2561.
Guidez F, Kevin Petrie P, Ford AM, Lu H, Bennett CA, MacGregor A et al. Recruitment of the nuclear receptor corepressor N-CoR by the TEL moiety of the childhood leukemia-associated TEL-AML1 oncoprotein. Blood. 2000 Oct 1;96(7):2557-2561.
Guidez, F. ; Kevin Petrie, Petrie ; Ford, A. M. ; Lu, H. ; Bennett, C. A. ; MacGregor, A. ; Hannemann, J. ; Ito, Y. ; Ghysdael, J. ; Greaves, M. ; Wiedemann, L. M. ; Zelent, Arthur Z. / Recruitment of the nuclear receptor corepressor N-CoR by the TEL moiety of the childhood leukemia-associated TEL-AML1 oncoprotein. In: Blood. 2000 ; Vol. 96, No. 7. pp. 2557-2561.
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abstract = "The t(12;21)(p13;q22) chromosomal translocation is the most frequent illegitimate gene recombination in a pediatric cancer and occurs in approximately 25{\%} of common acute lymphoblastic leukemia (cALL) cases. This rearrangement results in the in frame fusion of the 5'-region of the ETS-related gene, TEL (ETV6), to almost the entire acute myeloid leukemia 1 (AML 1)(also called CBFA2 or PEBP2AB1) locus and expression of the TEL-AML1 chimeric protein. Although AML1 stimulates transcription, TEL-AML1 functions as a repressor of some AML1 target genes. In contrast to the wild type AML1 protein, both TEL and TEL-AML1 interact with N-CoR, a component of the nuclear receptor compressor complex with histone deacetylase activity. The interaction between TEL and N-CoR requires the central region of TEL, which is retained in TEL-AML1, and TEL lacking this domain is impaired in transcriptional repression. Taken together, our results suggest that TEL-AML1 may contribute to leukemogenesis by recruiting N-CoR to AML1 target genes and thus imposing an altered pattern of their expression. (C) 2000 by the American Society of Hematology.",
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