Standard Article

Death Receptors

  1. Peter H Krammer,
  2. Inna N Lavrik

Published Online: 15 SEP 2009

DOI: 10.1002/9780470015902.a0021571

eLS

eLS

How to Cite

Krammer, P. H. and Lavrik, I. N. 2009. Death Receptors. eLS. .

Author Information

  1. German Cancer Research Center, Heidelberg, Germany

Publication History

  1. Published Online: 15 SEP 2009

This is not the most recent version of the article. View current version (14 DEC 2016)

Abstract

Apoptosis or programmed cell death is a common property of all multicellular organisms. It can be triggered by a number of factors including ultraviolet (UV) or γ-irradiation, chemotherapeutic drugs or growth factor withdrawal. A death signal can either be induced by death receptors (extrinsic pathway) or via the mitochondria (intrinsic pathway). The death receptor (DR) family is the subfamily of the tumour necrosis factor receptor (TNFR) superfamily. Stimulation of the death receptors results in the transduction of either apoptotic or survival signals. Here we present a general overview of death receptor signalling and describe the main mechanisms leading to activation of death receptor signalling pathways.

Key concepts:

  • Stimulation of the death receptors (DR) leads to apoptosis.

  • All DR are distinguished by the presence of the death domain.

  • Crosslinking of DR with death ligands results in formation of the death-inducing signalling complex (DISC).

  • Caspases play the central role in the transduction of death receptor apoptotic signal.

  • As a result of DISC formation procaspase-8 is activated with the formation of the active caspase-8 heterotetramer, which then triggers apoptotic signal.

  • c-FLIP proteins block caspase-8 activation at the DISC and thereby death receptor-induced apoptosis.

  • There are two types of apoptotic signalling: Type I and Type II cells.

  • Stimulation of DR also might lead to the induction of nonapoptotic pathways.

Keywords:

  • death receptors;
  • caspase;
  • death domain;
  • apoptosis