Necroptosis and its role in inflammation | Zendy

Manolis Pasparakis | Zendy; Peter Vandenabeele | Zendy

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Necroptosis and its role in inflammation

Author(s) -

Manolis Pasparakis,

Peter Vandenabeele

Publication year - 2015

Publication title -

nature

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 15.993

H-Index - 1226

eISSN - 1476-4687

pISSN - 0028-0836

DOI - 10.1038/nature14191

Subject(s) - necroptosis , ripk1 , inflammation , microbiology and biotechnology , programmed cell death , biology , trif , kinase , signal transduction , receptor , pathogenesis , tumor necrosis factor alpha , apoptosis , immunology , toll like receptor , innate immune system , genetics

Regulated cell death has essential functions in development and in adult tissue homeostasis. Necroptosis is a newly discovered pathway of regulated necrosis that requires the proteins RIPK3 and MLKL and is induced by death receptors, interferons, toll-like receptors, intracellular RNA and DNA sensors, and probably other mediators. RIPK1 has important kinase-dependent and scaffolding functions that inhibit or trigger necroptosis and apoptosis. Mouse-model studies have revealed important functions for necroptosis in inflammation and suggested that it could be implicated in the pathogenesis of many human inflammatory diseases. We discuss the mechanisms regulating necroptosis and its potential role in inflammation and disease.

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