FEBS Letters
Volume 583, Issue 17 , Pages 2758-2764, 3 September 2009

MCL-1ES, a novel variant of MCL-1, associates with MCL-1L and induces mitochondrial cell death

Edited by Barry Halliwell

  • Jae-Hong Kim

      Affiliations

    • Department of Biomedical Science, College of Life Science, CHA University, Seongnam 463-836, Republic of Korea
  • ,
  • Se-Hoon Sim

      Affiliations

    • Department of Life Science, Chung-Ang University, Seoul 156-756, Republic of Korea
  • ,
  • Hye-Jeong Ha

      Affiliations

    • Department of Life Science, Chung-Ang University, Seoul 156-756, Republic of Korea
  • ,
  • Jeong-Jae Ko

      Affiliations

    • Department of Biomedical Science, College of Life Science, CHA University, Seongnam 463-836, Republic of Korea
  • ,
  • Kangseok Lee

      Affiliations

    • Department of Life Science, Chung-Ang University, Seoul 156-756, Republic of Korea
    • Corresponding Author InformationCorresponding authors. Fax: +82 2 822 5241 (K. Lee), +82 31 725 8350 (J. Bae).
  • ,
  • Jeehyeon Bae

      Affiliations

    • Department of Biomedical Science, College of Life Science, CHA University, Seongnam 463-836, Republic of Korea
    • Corresponding Author InformationCorresponding authors. Fax: +82 2 822 5241 (K. Lee), +82 31 725 8350 (J. Bae).

Received 20 July 2009; received in revised form 5 August 2009; accepted 6 August 2009. published online 14 August 2009.

Abstract 

Myeloid cell leukemia-1 (MCL-1L) is a pro-survival member of the BCL-2 family that promotes cell survival. In this study, we identify a new splicing variant of human MCL-1 that encodes MCL-1ES (extra short). Sequence analysis indicates that this variant results from splicing within the first coding exon of MCL-1 at a non-canonical GC–AG donor–acceptor pair. The deduced sequence of MCL-1ES encodes a protein of 197 amino acids, and the PEST (proline, glutamic acid, serine, and threonine) motifs present in MCL-1L are absent. MCL-1ES interacts with MCL-1L and induces mitochondrial cell death, suggesting that alternative splicing of MCL-1 may control the fate of cells.

Structured summary

MINT-7255705, MINT-7255718, MINT-7255731, MINT-7255743:MCL1-ES (uniprotkb:Q07820-2) physically interacts (MI:0914) with MCL1-1L (uniprotkb:Q07820-1) by anti tag coimmunoprecipitation (MI:0007)

MINT-7255771:MCL1-ES (uniprotkb:Q07820-2) physically interacts (MI:0914) with Beta actin (uniprotkb:P60709) by anti tag coimmunoprecipitation (MI:0007)

MINT-7255781:MCL1-ES (uniprotkb:Q07820-2) physically interacts (MI:0914) with GAPDH (uniprotkb:P04406) by anti tag coimmunoprecipitation (MI:0007)

MINT-7255756:MCL1-ES (uniprotkb:Q07820-2) physically interacts (MI:0914) with COX IV (uniprotkb:P13073) by anti tag coimmunoprecipitation (MI:0007)

Keywords: Myeloid cell leukemia-1, MCL-1L, MCL-1 extra short, BCL-2 family, Apoptosis, Splicing variant

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PII: S0014-5793(09)00622-X

doi:10.1016/j.febslet.2009.08.006

FEBS Letters
Volume 583, Issue 17 , Pages 2758-2764, 3 September 2009