Matches in SemOpenAlex for { <https://semopenalex.org/work/W17144954> ?p ?o ?g. }
Showing items 1 to 44 of
44
with 100 items per page.
- W17144954 abstract "Inflammatory bowel disease is a chronic disease that causes inflammation of the intestine, and is one of the major health problems in the US. However, effective treatments remain to be explored. Understanding the mechanism of intestinal inflammation and damage will aid in effective treatments. TGF-β activated kinase 1 (TAK1), which is a member of the MAPKKK and is known to be activated by many different stressors and cytokines. We have previously shown that TAK1 deficiency in the intestinal epithelium causes oxidative damage including cell death and loss of paneth cells, which resemble IBD pathology. However, it was not known the mechanism of how reactive oxygen species (ROS) are accumulated and paneth cells are depleted. We tested a hypothesis that TAK1 signaling prevents commensal bacteria-induced ROS. We found that loss of bacteria or ablation of TLR signaling by MyD88 knockout could rescue the ROS accumulation in TAK1 deficient intestinal epithelium, while either of them could not restore the loss of paneth cells. We also identified that TAK1 modulates the stability of an antioxidant transcription factor Nrf2. These results suggest that TAK1 regulation of Nrf2 is important for elimination of bacteria-induced ROS in the intestine. Activation of TAK1 may be a possible new approach to reduce oxidative damage in the intestine. We are currently investigating the molecular mechanism of how TAK1 regulates paneth cells." @default.
- W17144954 created "2016-06-24" @default.
- W17144954 creator A5048107548 @default.
- W17144954 creator A5078826648 @default.
- W17144954 date "2012-04-01" @default.
- W17144954 modified "2023-10-16" @default.
- W17144954 title "TAK1 kinase signaling regulates Nrf2 and intestinal homeostasis" @default.
- W17144954 doi "https://doi.org/10.1096/fasebj.26.1_supplement.765.1" @default.
- W17144954 hasPublicationYear "2012" @default.
- W17144954 type Work @default.
- W17144954 sameAs 17144954 @default.
- W17144954 citedByCount "0" @default.
- W17144954 crossrefType "journal-article" @default.
- W17144954 hasAuthorship W17144954A5048107548 @default.
- W17144954 hasAuthorship W17144954A5078826648 @default.
- W17144954 hasConcept C184235292 @default.
- W17144954 hasConcept C62478195 @default.
- W17144954 hasConcept C63645605 @default.
- W17144954 hasConcept C86803240 @default.
- W17144954 hasConcept C95444343 @default.
- W17144954 hasConceptScore W17144954C184235292 @default.
- W17144954 hasConceptScore W17144954C62478195 @default.
- W17144954 hasConceptScore W17144954C63645605 @default.
- W17144954 hasConceptScore W17144954C86803240 @default.
- W17144954 hasConceptScore W17144954C95444343 @default.
- W17144954 hasIssue "S1" @default.
- W17144954 hasLocation W171449541 @default.
- W17144954 hasOpenAccess W17144954 @default.
- W17144954 hasPrimaryLocation W171449541 @default.
- W17144954 hasRelatedWork W1964810666 @default.
- W17144954 hasRelatedWork W1987621178 @default.
- W17144954 hasRelatedWork W2004726042 @default.
- W17144954 hasRelatedWork W2014713727 @default.
- W17144954 hasRelatedWork W2022448992 @default.
- W17144954 hasRelatedWork W2123013129 @default.
- W17144954 hasRelatedWork W2375538810 @default.
- W17144954 hasRelatedWork W2384817912 @default.
- W17144954 hasRelatedWork W2389717295 @default.
- W17144954 hasRelatedWork W3035328115 @default.
- W17144954 hasVolume "26" @default.
- W17144954 isParatext "false" @default.
- W17144954 isRetracted "false" @default.
- W17144954 magId "17144954" @default.
- W17144954 workType "article" @default.