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Tytuł pozycji:

Ubiquitin D Regulates IRE1alpha/c-Jun N-terminal Kinase (JNK) Protein-dependent Apoptosis in Pancreatic Beta Cells.

Tytuł :
Ubiquitin D Regulates IRE1alpha/c-Jun N-terminal Kinase (JNK) Protein-dependent Apoptosis in Pancreatic Beta Cells.
Index Terms :
Sciences bio-médicales et agricoles
Aged
Aged, 80 and over
Animals
Apoptosis
Blotting, Western
Cell Line
Cell Line, Tumor
Cells, Cultured
Cytokines -- pharmacology
Endoribonucleases -- genetics -- metabolism
Female
Gene Expression -- drug effects
HEK293 Cells
Humans
Insulin-Secreting Cells -- drug effects -- metabolism
JNK Mitogen-Activated Protein Kinases -- metabolism
Male
Middle Aged
Protein Binding
Protein-Serine-Threonine Kinases -- genetics -- metabolism
RNA Interference
Rats
Reverse Transcriptase Polymerase Chain Reaction
Ubiquitins -- genetics -- metabolism
Young Adult
IRE1α
apoptosis
c-Jun N-terminal kinase (JNK)
cytokinesis
endoplasmic reticulum stress (ER stress)
type 1 diabetes
ubiquitin D
info:eu-repo/semantics/article
info:ulb-repo/semantics/articlePeerReview
info:ulb-repo/semantics/openurl/article
Wydawca :
2016-06
Dodane szczegóły :
Brozzi, Flora
Gerlo, Sarah
Grieco, Fabio Arturo
Juusola, Matilda
Balhuizen, Alexander
Lievens, Sam
Gysemans, Conny
Bugliani, Marco
Mathieu, Chantal
Marchetti, Piero
Tavernier, Jan
Eizirik, Decio
Typ dokumentu :
Zasób elektroniczny
URL :
http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/231862">http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/231862
http://worldcat.org/search?q=on:EQY+http://difusion-oai.ulb.ac.be/oai/request+DCG_ENTIRE_REPOSITORY+CNTCOLL">http://worldcat.org/search?q=on:EQY+http://difusion-oai.ulb.ac.be/oai/request+DCG_ENTIRE_REPOSITORY+CNTCOLL
Dostępność :
Open access content. Open access content
1 full-text file(s): info:eu-repo/semantics/restrictedAccess
Pozostałe numery :
EQY oai:dipot.ulb.ac.be:2013/231862
961109553
Źródło wspomagające :
UNIV LIBR DE BRUXELLES
From OAIster®, provided by the OCLC Cooperative.
Numer akcesji :
edsoai.ocn961109553
Zasób elektroniczny
Pro-inflammatory cytokines contribute to pancreatic beta cell apoptosis in type 1 diabetes at least in part by inducing endoplasmic reticulum (ER) stress and the consequent unfolded protein response (UPR). It remains to be determined what causes the transition from "physiological" to "apoptotic" UPR, but accumulating evidence indicates that signaling by the ER transmembrane protein IRE1α is critical for this transition. IRE1α activation is regulated by both intra-ER and cytosolic cues. We evaluated the role for the presently discovered cytokine-induced and IRE1α-interacting protein ubiquitin D (UBD) on the regulation of IRE1α and its downstream targets. UBD was identified by use of a MAPPIT (mammalian protein-protein interaction trap)-based IRE1α interactome screen followed by comparison against functional genomic analysis of human and rodent beta cells exposed to pro-inflammatory cytokines. Knockdown of UBD in human and rodent beta cells and detailed signal transduction studies indicated that UBD modulates cytokine-induced UPR/IRE1α activation and apoptosis. UBD expression is induced by the pro-inflammatory cytokines interleukin (IL)-1β and interferon (IFN)-γ in rat and human pancreatic beta cells, and it is also up-regulated in beta cells of inflamed islets from non-obese diabetic mice. UBD interacts with IRE1α in human and rodent beta cells, modulating IRE1α-dependent activation of JNK and cytokine-induced apoptosis. Our data suggest that UBD provides a negative feedback on cytokine-induced activation of the IRE1α/JNK pro-apoptotic pathway in cytokine-exposed beta cells.
info:eu-repo/semantics/published

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