PELI3
Gene Ontology Biological Process
- defense response to Gram-negative bacterium [IMP]
- negative regulation of Toll signaling pathway [IGI]
- negative regulation of extrinsic apoptotic signaling pathway [IMP, ISO]
- negative regulation of protein ubiquitination [IGI]
- negative regulation of tumor necrosis factor-mediated signaling pathway [IMP, ISO]
- negative regulation of type I interferon production [IMP]
- positive regulation of nucleotide-binding oligomerization domain containing 2 signaling pathway [IMP]
- protein K63-linked ubiquitination [IDA]
- protein ubiquitination [IMP]
- regulation of nucleotide-binding oligomerization domain containing 1 signaling pathway [IMP]
Gene Ontology Molecular Function
UBC
Gene Ontology Biological Process
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Affinity Capture-Western
An interaction is inferred when a bait protein is affinity captured from cell extracts by either polyclonal antibody or epitope tag and the associated interaction partner identified by Western blot with a specific polyclonal antibody or second epitope tag. This category is also used if an interacting protein is visualized directly by dye stain or radioactivity. Note that this differs from any co-purification experiment involving affinity capture in that the co-purification experiment involves at least one extra purification step to get rid of potential contaminating proteins.
Publication
Autophagy-dependent PELI3 degradation inhibits proinflammatory IL1B expression.
Lipopolysaccharide (LPS)-induced activation of TLR4 (toll-like receptor 4) is followed by a subsequent overwhelming inflammatory response, a hallmark of the first phase of sepsis. Therefore, counteracting excessive innate immunity by autophagy is important to contribute to the termination of inflammation. However, the exact molecular details of this interplay are only poorly understood. Here, we show that PELI3/Pellino3 (pellino E3 ubiquitin ... [more]
Throughput
- Low Throughput
Curated By
- BioGRID