Contribution of the Unfolded Protein Response (UPR) to the Pathogenesis of Proteasome-Associated Autoinflammatory Syndromes (PRAAS)

Journal
Frontiers in Immunology
ISSN
1664-3224
Date Issued
2019
Author(s)
Frédéric Ebstein
Maja Studencka-Turski
Elke Krüger
Type
Resource Types::text::journal::journal article
Scopus ID
2-s2.0-85076493974
WoS ID
WOS:000502097100001
DOI
URL
URL Institutional Repository
Cite this document
Ebstein, F., Poli Harlowe, M. C., Studencka-Turski, M., & Krüger, E. (2019). Contribution of the unfolded protein response (Upr) to the pathogenesis of proteasome-associated autoinflammatory syndromes(Praas). Frontiers in Immunology, 10, 2756. https://doi.org/10.3389/fimmu.2019.02756
Project(s)
Subjects
proteasome

; 

er stress

; 

unfolded protein response

; 

mtorc1

; 

tcf11

; 

nrf1

; 

autoinflammation

; 

activating transcription factor 6

; 

animals

; 

autoimmune diseases

; 

eif-2 kinase

; 

endoplasmic reticulum

; 

endoribonucleases

; 

humans

; 

interferon type i

; 

mutation

; 

nf-e2-related factor 1

; 

proteasome endopeptidase complex

; 

protein multimerization

; 

protein-serine-threonine kinases

; 

receptor cross-talk

; 

syndrome

; 

unfolded protein response

; 

activating transcription factor 6

; 

beta interferon

; 

biological marker

; 

gamma interferon inducible protein 10

; 

initiation factor 2

; 

mammalian target of rapamycin complex 1

; 

messenger rna

; 

mitochondrial dna

; 

mitogen activated protein kinase

; 

proteasome

; 

protein kinase r

; 

sterol regulatory element binding protein

; 

stress activated protein kinase

; 

tunicamycin

; 

x box binding protein 1

; 

activating transcription factor 6

; 

atf6 protein, human

; 

ern1 protein, human

; 

interferon

; 

nfe2l1 protein, human

; 

perk kinase

; 

proteasome

; 

protein kinase r

; 

protein serine threonine kinase

; 

ribonuclease

; 

transcription factor nrf1

; 

autoinflammatory disease

; 

citric acid cycle

; 

cognitive defect

; 

endoplasmic reticulum stress

; 

gene expression

; 

gene mutation

; 

genetic variability

; 

homeostasis

; 

human

; 

innate immunity

; 

lipid metabolism

; 

lipodystrophy

; 

loss of function mutation

; 

nonhuman

; 

open reading frame

; 

oxidative stress

; 

phenotype

; 

proteasome associated autoinflammatory syndrome

; 

protein degradation

; 

protein phosphorylation

; 

protein synthesis

; 

review

; 

signal transduction

; 

tumor necrosis factor receptor associated periodic syndrome

; 

ubiquitination

; 

unfolded protein response

; 

upregulation

; 

animal

; 

autoimmune disease

; 

endoplasmic reticulum

; 

genetics

; 

immunology

; 

metabolism

; 

mutation

; 

protein multimerization

; 

receptor cross-talk

; 

syndrome

; 

unfolded protein response