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Initiation of Apaf-1 translation by internal ribosome entry

M J Coldwell1, S A Mitchell, M Stoneley

  • 1Department of Biochemistry, University of Leicester, University Road, Leicester LE1 7RH.

Oncogene
|March 7, 2000
PubMed

Insights

The apoptotic protease activating factor (Apaf-1) mRNA uses internal ribosome entry sites (IRES) for translation initiation. This mechanism ensures constant Apaf-1 protein levels, even when cap-dependent translation is impaired.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Apoptotic protease activating factor (Apaf-1) is crucial for apoptosis, mediating caspase-9 activation.
  • The 5' untranslated region (UTR) of Apaf-1 mRNA is long, G-C rich, and forms secondary structures.
  • Translation initiation mechanisms for regulatory proteins are critical for cellular function.

Purpose of the Study:

  • To investigate the translation initiation mechanism of Apaf-1 mRNA.
  • To identify and characterize the internal ribosome entry segment (IRES) within the Apaf-1 5' UTR.
  • To determine the functional significance of Apaf-1 IRES activity in various human cell types.

Main Methods:

  • Identification of the internal ribosome entry segment (IRES) within the 233-nucleotide region of the Apaf-1 5' UTR.
  • Assays to measure the activity of the Apaf-1 IRES in different human cell lines (HeLa, HepG2, MCF7, HK293, COS7, MRC5).
  • Comparative analysis of Apaf-1 IRES activity against known IRES elements (HRV, c-myc).

Main Results:

  • The 5' UTR of Apaf-1 contains a functional internal ribosome entry segment (IRES).
  • Apaf-1 IRES-mediated translation initiation was observed in multiple human cell types.
  • Apaf-1 IRES activity is comparable to HRV IRES but less active than c-myc IRES.

Conclusions:

  • Apaf-1 mRNA translation is initiated exclusively via an IRES mechanism.
  • The Apaf-1 IRES ensures constitutive expression of Apaf-1 protein.
  • This IRES-dependent translation provides a constant Apaf-1 level, vital under conditions inhibiting cap-dependent translation.

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