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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 

Posttranslational modification of TEL and TEL/ AML1 by SUMO-1 and cell-cycle-dependent assembly into nuclear bodies.

The E-26 transforming specific (ETS)-related gene, TEL, also known as ETV6, encodes a strong transcription repressor that is rearranged in several recurring chromosomal rearrangements associated with leukemia and congenital fibrosarcoma. TEL is a nuclear phosphoprotein that is widely expressed in all normal tissues. TEL contains a DNA-binding domain at the C terminus and a helix-loop-helix domain (also called a pointed domain) at the N terminus. The pointed domain is necessary for homotypic dimerization and for interaction with the ubiquitin-conjugating enzyme UBC9. Here we show that the interaction with UBC9 leads to modification of TEL by conjugating it to SUMO-1. The SUMO-1- modified TEL localizes to cell-cycle-specific nuclear speckles that we named TEL bodies. We also show that the leukemia-associated fusion protein TEL/ AML1 is modified by SUMO-1 and found in the TEL bodies, in a pattern quite different from what we observe and report for AML1. Therefore, SUMO-1 modification of TEL could be a critical signal necessary for normal functioning of the protein. In addition, the modification by SUMO-1 of TEL/ AML1 could lead to abnormal localization of the fusion protein, which could have consequences that include contribution to neoplastic transformation.[1]

References

  1. Posttranslational modification of TEL and TEL/AML1 by SUMO-1 and cell-cycle-dependent assembly into nuclear bodies. Chakrabarti, S.R., Sood, R., Nandi, S., Nucifora, G. Proc. Natl. Acad. Sci. U.S.A. (2000)
 
 
 
 
 
 
 
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