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Interactions between the leukaemia-associated ETO homologues of nuclear repressor proteins.

Rondin Lindberg, Sofia LU ; Olsson, André LU ; Persson, Ann-Maj LU and Olsson, Inge LU (2003) In European Journal of Haematology1987-01-01+01:00 71(6). p.439-447
Abstract
The eight-twenty-one (ETO) homologues, represented by ETO, myeloid transforming gene-related protein 1 (MTGR1) and myeloid transforming gene chromosome 16 (MTG16), are nuclear repressor proteins. ETO is part of the fusion protein acute myeloid leukaemia (AML)1-ETO, resulting from the translocation (8;21). Similarly, MTG16 is disrupted to become part of AML1/MTG16 in t(16;21). The aberrant expression of these chimeras could affect interplay between ETO homologues and contribute to the leukaemogenic process. We investigated possible interactions between the ETO homologues. Ectopic co-expression in COS-cells resulted in heterodimerisation of the various ETO homologues suggesting that they may co-operate. Similarly, the chimeric oncoprotein... (More)
The eight-twenty-one (ETO) homologues, represented by ETO, myeloid transforming gene-related protein 1 (MTGR1) and myeloid transforming gene chromosome 16 (MTG16), are nuclear repressor proteins. ETO is part of the fusion protein acute myeloid leukaemia (AML)1-ETO, resulting from the translocation (8;21). Similarly, MTG16 is disrupted to become part of AML1/MTG16 in t(16;21). The aberrant expression of these chimeras could affect interplay between ETO homologues and contribute to the leukaemogenic process. We investigated possible interactions between the ETO homologues. Ectopic co-expression in COS-cells resulted in heterodimerisation of the various ETO homologues suggesting that they may co-operate. Similarly, the chimeric oncoprotein AML1-ETO interacted with both MTGR1 and MTG16. However, results from cell lines endogenously expressing more than one ETO homologue did not demonstrate co-precipitation. Results from IP-Western and size determination by gel filtration of deletion mutants expressed in COS-cells, indicated an important role of the HHR domain for oligomerisation. A role was also suggested for the Nervy domain in the homologue interactions. Our results suggest that ETO homologues can interact with each other as well as with AML1-ETO, although it is unclear as to what extent these interactions occur in vivo. (Less)
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published
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European Journal of Haematology1987-01-01+01:00
volume
71
issue
6
pages
439 - 447
publisher
Wiley-Blackwell
external identifiers
  • wos:000186434900007
  • scopus:0344961717
ISSN
1600-0609
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English
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yes
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f208afd9-1a0b-4c5e-8eaf-2807cab34827 (old id 119324)
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http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14703694&dopt=Abstract
date added to LUP
2007-07-09 13:16:57
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2018-05-29 09:59:49
@article{f208afd9-1a0b-4c5e-8eaf-2807cab34827,
  abstract     = {The eight-twenty-one (ETO) homologues, represented by ETO, myeloid transforming gene-related protein 1 (MTGR1) and myeloid transforming gene chromosome 16 (MTG16), are nuclear repressor proteins. ETO is part of the fusion protein acute myeloid leukaemia (AML)1-ETO, resulting from the translocation (8;21). Similarly, MTG16 is disrupted to become part of AML1/MTG16 in t(16;21). The aberrant expression of these chimeras could affect interplay between ETO homologues and contribute to the leukaemogenic process. We investigated possible interactions between the ETO homologues. Ectopic co-expression in COS-cells resulted in heterodimerisation of the various ETO homologues suggesting that they may co-operate. Similarly, the chimeric oncoprotein AML1-ETO interacted with both MTGR1 and MTG16. However, results from cell lines endogenously expressing more than one ETO homologue did not demonstrate co-precipitation. Results from IP-Western and size determination by gel filtration of deletion mutants expressed in COS-cells, indicated an important role of the HHR domain for oligomerisation. A role was also suggested for the Nervy domain in the homologue interactions. Our results suggest that ETO homologues can interact with each other as well as with AML1-ETO, although it is unclear as to what extent these interactions occur in vivo.},
  author       = {Rondin Lindberg, Sofia and Olsson, André and Persson, Ann-Maj and Olsson, Inge},
  issn         = {1600-0609},
  language     = {eng},
  number       = {6},
  pages        = {439--447},
  publisher    = {Wiley-Blackwell},
  series       = {European Journal of Haematology1987-01-01+01:00},
  title        = {Interactions between the leukaemia-associated ETO homologues of nuclear repressor proteins.},
  url          = {http://dx.doi.org/},
  volume       = {71},
  year         = {2003},
}