Informacja

Drogi użytkowniku, aplikacja do prawidłowego działania wymaga obsługi JavaScript. Proszę włącz obsługę JavaScript w Twojej przeglądarce.

Przeglądasz jako GOŚĆ
Tytuł pozycji:

RNA-sequencing identifies dysregulation of the human pancreatic islet transcriptome by the saturated fatty acid palmitate.

Tytuł :
RNA-sequencing identifies dysregulation of the human pancreatic islet transcriptome by the saturated fatty acid palmitate.
Index Terms :
Biologie
Biologie moléculaire
Biologie cellulaire
Biologie générale
Diabétologie
Animals
Apoptosis -- drug effects -- genetics
Blotting, Western
Cell Line
Cells, Cultured
Diabetes Mellitus, Type 2 -- genetics -- metabolism
Endoplasmic Reticulum Stress -- drug effects -- genetics
Female
Gene Expression Regulation, Enzymologic
Genetic Predisposition to Disease
Humans
Inflammation -- genetics -- metabolism
Islets of Langerhans -- drug effects -- metabolism
Male
Palmitates -- metabolism
Sequence Analysis, RNA
Signal Transduction
Transcriptome
info:eu-repo/semantics/article
info:ulb-repo/semantics/articlePeerReview
info:ulb-repo/semantics/openurl/article
Wydawca :
2014
Dodane szczegóły :
Cnop, Miriam
Abdulkarim, Baroj
Bottu, Guy
Andrade Da Cunha, Daniel
Igoillo Esteve, Mariana
Masini, Matilde
Turatsinze, Jean Valéry
Griebel, Thasso
Villate, Olatz
Santin Gomez, Izortze
Bugliani, Marco
Ladrière, Laurence
Marselli, Lorella
McCarthy, Mark I
Marchetti, Piero
Sammeth, Michael
Eizirik, Decio L.
Typ dokumentu :
Zasób elektroniczny
URL :
http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/154918">http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/154918
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/openAccess
Pozostałe numery :
EQY oai:dipot.ulb.ac.be:2013/154918
uri/info:doi/10.2337/db13-1383
uri/info:pii/db13-1383
uri/info:pmid/24379348
uri/info:scp/84900334812
https://dipot.ulb.ac.be/dspace/bitstream/2013/154918/3/doi_139695.pdf
872083858
Źródło wspomagające :
UNIV LIBR DE BRUXELLES
From OAIster®, provided by the OCLC Cooperative.
Numer akcesji :
edsoai.ocn872083858
Zasób elektroniczny
Pancreatic β-cell dysfunction and death are central in the pathogenesis of type 2 diabetes. Saturated fatty acids cause β-cell failure and contribute to diabetes development in genetically predisposed individuals.Here we used RNA-sequencing to map transcripts expressed in five palmitate-treated human islet preparations, observing 1,325 modified genes. Palmitate induced fatty acid metabolism and endoplasmic reticulum (ER) stress. Functional studies identified novel mediators of adaptive ER stress signaling. Palmitate modified genes regulating ubiquitin and proteasome function, autophagy and apoptosis. Inhibition of autophagic flux and lysosome function contributed to lipotoxicity. Palmitate inhibited transcription factors controlling β-cell phenotype including PAX4 and GATA6. 59 type 2 diabetes candidate genes were expressed in human islets, and 11 were modified by palmitate. Palmitate modified expression of 17 splicing factors and shifted alternative splicing of 3,525 transcripts. Ingenuity Pathway Analysis of modified transcripts and genes confirmed that top changed functions related to cell death. DAVID analysis of transcription binding sites in palmitate-modified transcripts revealed a role for PAX4, GATA and the ER stress response regulators XBP1 and ATF6.This human islet transcriptome study identified novel mechanisms of palmitate-induced β-cell dysfunction and death. The data point to crosstalk between metabolic stress and candidate genes at the β-cell level.
JOURNAL ARTICLE
SCOPUS: ar.j
info:eu-repo/semantics/published

Ta witryna wykorzystuje pliki cookies do przechowywania informacji na Twoim komputerze. Pliki cookies stosujemy w celu świadczenia usług na najwyższym poziomie, w tym w sposób dostosowany do indywidualnych potrzeb. Korzystanie z witryny bez zmiany ustawień dotyczących cookies oznacza, że będą one zamieszczane w Twoim komputerze. W każdym momencie możesz dokonać zmiany ustawień dotyczących cookies