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A novel splicing variant of mouse interleukin (IL)-24 antagonizes IL-24-induced apoptosis

Anupama Sahoo1, Yun Min Jung, Ho-Keun Kwon

  • 1Department of Life Sciences, Gwangju Institute of Science and Technology, Gwangju 500-712, Korea.

The Journal of Biological Chemistry
|August 19, 2008
PubMed

Insights

A novel splice variant, FISP-sp, derived from the Interleukin-24/FISP gene, inhibits FISP

Area of Science:

  • Molecular Biology
  • Immunology
  • Cell Biology

Background:

  • Alternative mRNA splicing diversifies protein function from a single gene.
  • Interleukin-24 (IL-24) is part of the IL-10 gene family.
  • FISP (IL-4-induced secreted protein) is the murine homologue of IL-24, secreted by T helper 2 lymphocytes.

Purpose of the Study:

  • To characterize a novel splice variant of mouse IL-24/FISP, termed FISP-sp.
  • To investigate the functional and localization properties of FISP-sp.
  • To determine the interaction between FISP-sp and the primary FISP protein.

Main Methods:

  • Identification and characterization of the FISP-sp splice variant.
  • Analysis of FISP-sp expression levels and localization.
  • Assessment of FISP-sp's effect on FISP-induced growth inhibition and apoptosis.
  • Investigation of FISP-sp's interaction with FISP and its impact on secretion.

Main Results:

  • A novel splice variant, FISP-sp, was identified, lacking 29 nucleotides from exon 4 of FISP.
  • FISP-sp is expressed at 10% of total FISP transcription levels and localized exclusively in the endoplasmic reticulum.
  • FISP-sp does not induce growth inhibition or apoptosis; its expression is upregulated by endoplasmic reticulum stress.
  • FISP-sp dimerizes with FISP, blocking its secretion and inhibiting FISP-induced apoptosis in vivo.

Conclusions:

  • The novel splice variant FISP-sp acts as a negative regulator of the primary FISP protein.
  • FISP-sp interferes with FISP secretion and function, thereby modulating apoptosis.
  • Endoplasmic reticulum stress influences the expression of FISP-sp, suggesting a role in cellular stress responses.

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