Back to search

Article

An epithelial <i>Nfkb2</i> pathway exacerbates intestinal inflammation by supplementing latent RelA dimers to the canonical NF-κB module

2020-11-02

Abstract excerpt

Aberrant inflammation associated with human ailments, including inflammatory bowel disease (IBD), is typically fuelled by the inordinate activity of RelA/NF-κB transcription factors. As such, the canonical NF-κB module mediates controlled nuclear activation of RelA dimers from the latent cytoplasmic complexes. What provokes pathological RelA activity in the colitogenic gut remains unclear. The noncanonical NF-κB p...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work
fdc47903-6499-548a-9b85-c0bb21a162a4
DOI
10.1101/2020.11.02.365890
Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest
Interactive article relationship graphSelect a related publication card to move it into the centre and load its closest explainable connections. Solid lines are source-backed structured connections. Dashed lines are semantic discovery signals and are not scientific evidence.
An epithelial <i>Nfkb2</i> pathway exacerbates intestinal inflammation by supplementing latent RelA dimers to the canonical NF-κB moduleDOI 10.1101/2020.11.02.365890
Select a neighboring publication to make it the new centre.