Asset Details
Do you wish to reserve the book?
RORα is crucial for attenuated inflammatory response to maintain intestinal homeostasis
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
RORα is crucial for attenuated inflammatory response to maintain intestinal homeostasis
Do you wish to request the book?
RORα is crucial for attenuated inflammatory response to maintain intestinal homeostasis
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
RORα is crucial for attenuated inflammatory response to maintain intestinal homeostasis
2019
Overview
Retinoic acid-related orphan receptor α (RORα) functions as a transcription factor for various biological processes, including circadian rhythm, cancer, and metabolism. Here, we generate intestinal epithelial cell (IEC)-specific RORα-deficient (RORαΔIEC) mice and find that RORα is crucial for maintaining intestinal homeostasis by attenuating nuclear factor κB (NF-κB) transcriptional activity. RORαΔIEC mice exhibit excessive intestinal inflammation and highly activated inflammatory responses in the dextran sulfate sodium (DSS) mouse colitis model. Transcriptome analysis reveals that deletion of RORα leads to up-regulation of NF-κB target genes in IECs. Chromatin immunoprecipitation analysis reveals corecruitment of RORα and histone deacetylase 3 (HDAC3) on NF-κB target promoters and subsequent dismissal of CREB binding protein (CBP) and bromodomaincontaining protein 4 (BRD4) for transcriptional repression. Together, we demonstrate that RORα/HDAC3-mediated attenuation of NF-κB signaling controls the balance of inflammatory responses, and therapeutic strategies targeting this epigenetic regulation could be beneficial to the treatment of chronic inflammatory diseases, including inflammatory bowel disease (IBD).
Publisher
National Academy of Sciences
Subject
/ Colitis
/ Colon
/ Cyclic AMP response element-binding protein
/ Dextran
/ Epigenesis, Genetic - physiology
/ Epithelial Cells - metabolism
/ Epithelial Cells - physiology
/ Female
/ Mice
/ Orphan Nuclear Receptors - metabolism
/ Proteins
/ Sodium
/ Transcription Factors - metabolism
