Impact of inhibitor of apoptosis proteins on immune modulation and inflammation.

Sharma, Sachin; Kaufmann, Thomas; Biswas, Subhrajit (2017). Impact of inhibitor of apoptosis proteins on immune modulation and inflammation. Immunology and cell biology, 95(3), pp. 236-243. Nature Publishing Group 10.1038/icb.2016.101

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The routes leading to programmed cell death are as tightly regulated as those of cellular growth and proliferation, and a finely synchronized balance between the life and death of cells ensures proper organ size and function. Inhibitors of apoptosis (IAPs) proteins were initially characterized by their ability to directly bind and inhibit apoptotic caspases. However, recent studies have clarified that IAPs are much more functionally versatile, modulating a vast range of signaling pathways that have an impact on antimicrobial responses, tumorigenesis, metastasis and cellular migration. A significant contribution of IAPs in tumorigenesis is their inherent function as E3 ubiquitin ligases to modulate cellular signaling downstream of death receptors or certain pattern recognition receptors. In this review, we focus on modulation of the innate and adaptive immune systems, macrophage plasticity and inflammatory responses by IAP family members. We also explore the rationale to target IAPs pharmacologically for the treatment of a number of inflammatory diseases and cancer.Immunology and Cell Biology accepted article preview online, 07 October 2016. doi:10.1038/icb.2016.101.

Item Type:

Journal Article (Review Article)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Pharmacology

UniBE Contributor:

Kaufmann, Thomas

Subjects:

600 Technology > 610 Medicine & health

ISSN:

0818-9641

Publisher:

Nature Publishing Group

Language:

English

Submitter:

Debora Scherrer

Date Deposited:

20 Oct 2017 09:39

Last Modified:

23 Oct 2017 16:34

Publisher DOI:

10.1038/icb.2016.101

PubMed ID:

27713393

BORIS DOI:

10.7892/boris.89259

URI:

https://boris.unibe.ch/id/eprint/89259

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