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In Vitro 2010

Identification of DELE, a novel DAP3-binding protein which is crucial for death receptor-mediated apoptosis induction

Harada, Tanenobu; Iwai, Atsushi; Miyazaki, Tadaaki · Apoptosis · DOI: 10.1007/s10495-010-0519-3
Research Archive
TL;DR — Key Findings
  • DELE binds DAP3 and supports death-receptor apoptosis signaling.
  • DELE knockdown reduced activation of several caspases.
  • This is indirect background, not beta-glucan evidence.

Abstract

A yeast two-hybrid screen identified DELE as a protein that binds death-associated protein 3 (DAP3), and the interaction was confirmed in mammalian cells. DELE expression increased susceptibility to TNF-alpha- and TRAIL-induced apoptosis, while DELE knockdown reduced apoptosis and caspase-3, -8, and -9 activation after death-receptor stimulation. The study defines a cell-death signaling mechanism. It did not investigate beta-glucan or Aureobasidium pullulans.

Summary

Summary

Study

DELE was identified and tested as a DAP3-binding protein in death-receptor signaling.

Finding

DELE supported TNF-alpha-, Fas-, and TRAIL-related caspase activation and apoptosis.

Limit

No beta-glucan or Aureobasidium intervention was studied.

AI-generated summary for accessibility. Always refer to the original paper.

Citation

Harada, Tanenobu; Iwai, Atsushi; Miyazaki, Tadaaki. Identification of DELE, a novel DAP3-binding protein which is crucial for death receptor-mediated apoptosis induction. Apoptosis. 2010. DOI: 10.1007/s10495-010-0519-3.

Study Details
Study Type
In Vitro
Published
2010
Journal
Apoptosis
Authors
Harada, Tanenobu; Iwai, Atsushi; Miyazaki, Tadaaki
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