Inhibitor of apoptosis proteins in human health and disease

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61988987%3A17110%2F19%3AA200212U" target="_blank" >RIV/61988987:17110/19:A200212U - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00843989:_____/19:E0108118

Výsledek na webu

<a href="https://www.nature.com/articles/s41435-019-0078-8" target="_blank" >https://www.nature.com/articles/s41435-019-0078-8</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1038/s41435-019-0078-8" target="_blank" >10.1038/s41435-019-0078-8</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Inhibitor of apoptosis proteins in human health and disease

Popis výsledku v původním jazyce

The inhibitor of apoptosis proteins (IAPs) are best known for their ability to regulate cell survival and death processes. However, in addition to cell death, IAPs also act as innate immune sensors and modulate multiple pathways, such as autophagy and cell division. Many of these IAP functions are non-redundant even though they are based on the same molecular mechanism of action. These distinct functions of IAPs derive from their capacity to target specific substrates for ubiquitination and/or proteolytic cleavage. The unique functions of IAPs also derives from their unique cellular localizations, cell type and tissue-specific expression patterns. The diverse roles of IAPs are reflected by the fact that in humans the IAP family comprises eight distinct members. Genetic evidence from human pathologies also attests to the non-redundant functions of the IAPs since very diverse diseases arise upon aberrant IAP expression. In this review, we give an overview of the known mechanisms of action of the various IAPs, and focus on their specific roles in mediating innate immunity. We also look at the distinct phenotypes related to the dysregulation of the IAPs, and the human pathologies associated with each human IAP.

Název v anglickém jazyce

Inhibitor of apoptosis proteins in human health and disease

Popis výsledku anglicky

The inhibitor of apoptosis proteins (IAPs) are best known for their ability to regulate cell survival and death processes. However, in addition to cell death, IAPs also act as innate immune sensors and modulate multiple pathways, such as autophagy and cell division. Many of these IAP functions are non-redundant even though they are based on the same molecular mechanism of action. These distinct functions of IAPs derive from their capacity to target specific substrates for ubiquitination and/or proteolytic cleavage. The unique functions of IAPs also derives from their unique cellular localizations, cell type and tissue-specific expression patterns. The diverse roles of IAPs are reflected by the fact that in humans the IAP family comprises eight distinct members. Genetic evidence from human pathologies also attests to the non-redundant functions of the IAPs since very diverse diseases arise upon aberrant IAP expression. In this review, we give an overview of the known mechanisms of action of the various IAPs, and focus on their specific roles in mediating innate immunity. We also look at the distinct phenotypes related to the dysregulation of the IAPs, and the human pathologies associated with each human IAP.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10601 - Cell biology

Projekt

<a href="/cs/project/GJ18-24070Y" target="_blank" >GJ18-24070Y: Analýza souhry ubikvitinace a fosforylace v onkogenní signalizaci proteinu MyD88 pro identifikaci nových možností v terapii lymfomů</a><br>

Návaznosti

V - Vyzkumna aktivita podporovana z jinych verejnych zdroju

Rok uplatnění

2019

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Genes & Immunity

ISSN

1466-4879

e-ISSN

1476-5470

Svazek periodika

20

Číslo periodika v rámci svazku

8

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

9

Strana od-do

641-650

Kód UT WoS článku

000499163100004

EID výsledku v databázi Scopus

2-s2.0-85066105279