Cytoplasmic Suppression of Inflammatory Signaling
Abstract
The anti-inflammatory protein ABIN-1 (also known as TNIP1), independently and together with one of its binding partners, A20, has been linked to limiting inflammatory bowel disease(IBD). Cells deficient in ABIN-1/TNIP1 mount an excessive inflammatory response because they are hypersensitive to debris shed from bacteria; ABIN-1 suppresses cytoplasmic signaling leading to inflammation. Our data in the original application, previous award supported data publication, and recently published review confirm and extend our hypothesis: conformational flexibility for ABIN-1 affects its function, including in multiple, relevant cell types. ABIN-1 flexibility helps resolve i) how it interacts with diverse partners, ii)its relatively short half-life during inflammation, and iii) what characteristics about it could be co-opted for future studies of its anti-inflammatory capacity. New data on theABIN-1 protein flexibility is presented here for the reporting period.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 2023
- Accession Number
- AD1217460
Entities
People
- Brian Aneskievich
Organizations
- University of Connecticut