Cytoplasmic Suppression of Inflammatory Signaling
Abstract
The anti-inflammatory protein ABIN-1 (also referred to as TNIP1), independently and together with one of its binding partners, A20, has been linked to inflammatory bowel disease (IBD).Cells deficient in ABIN-1/TNIP1 mount an excessive inflammatory response because they are hypersensitive to debris shed from bacteria. Thus ABIN-1 suppresses cytoplasmic signaling steps leading to inflammation. Our data submitted with the original application and award supported publication stemming provide new findings for to confirm and extend our hypothesis of that conformational flexibility for ABIN-1 is likely to affects its function. This concept of flexibility helps resolve i) how ABIN-1 interacts with its diverse protein partners, ii) the relatively short duration time of ABIN-1 protein during inflammation, andiii) what protein characteristics about it could be co-opted for future cell-based studies of its anti-inflammatory capacity.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 2022
- Accession Number
- AD1190530
Entities
People
- Brian Aneskievich
Organizations
- University of Connecticut