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Proteome analysis reveals new mechanisms of Bcl11b-loss driven apoptosis

Narasimha Kumar Karanam1, Piotr Grabarczyk, Elke Hammer

  • 1Interfakultäres Institut für Genetik und Funktionelle Genomforschung, Ernst-Moritz-Arndt-Universität Greifswald, Germany.

Journal of Proteome Research
|June 2, 2010
PubMed

Insights

Bcl11b protein depletion triggers programmed cell death in malignant T cells via the mitochondrial pathway. This study reveals new mechanisms of cell death and cell cycle disruption following BCL11B down-regulation.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Proteomics

Background:

  • Bcl11b protein is crucial for T cell development, nervous system function, and DNA repair.
  • Down-regulation of BCL11B induces apoptosis in malignant T cells, but the precise mechanisms remain unclear.

Purpose of the Study:

  • To investigate the role of Bcl11b in malignant T cell lines (Jurkat, huT78).
  • To elucidate the molecular mechanisms underlying Bcl11b depletion-induced cell death and cell cycle disturbances.

Main Methods:

  • Two-dimensional difference in-gel electrophoresis (2D-DIGE)
  • Mass spectrometry
  • Cell biological experiments

Main Results:

  • Evidence supports the involvement of the mitochondrial apoptotic pathway.
  • Cleavage of caspase targets (myosin, spectrin, vimentin) and upregulation/phosphorylation of ERM proteins were observed.
  • Increased levels of proteins involved in cell cycle entry (DUT-N, CDK6, MCM4, MCM6, MAT1) were detected.

Conclusions:

  • Bcl11b depletion activates the mitochondrial apoptotic pathway in malignant T cells.
  • ERM protein regulation and cell cycle protein alterations contribute to cell death and disturbances.
  • This research provides novel insights into the mechanisms of cell death and cell cycle disruption caused by Bcl11b loss.

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