FBXO22 inhibits colitis and colorectal carcinogenesis by regulating the degradation of the S2448-phosphorylated form of mTOR.
Animals
TOR Serine-Threonine Kinases
/ metabolism
Colorectal Neoplasms
/ metabolism
Colitis
/ metabolism
Mice
Humans
F-Box Proteins
/ metabolism
Mice, Knockout
Phosphorylation
Proteolysis
/ drug effects
Azoxymethane
/ toxicity
Carcinogenesis
/ metabolism
Dextran Sulfate
/ toxicity
Receptors, Cytoplasmic and Nuclear
FBXO22
colitis
colorectal carcinogenesis
pS2448-mTOR
Journal
Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876
Informations de publication
Date de publication:
05 Nov 2024
05 Nov 2024
Historique:
medline:
1
11
2024
pubmed:
1
11
2024
entrez:
1
11
2024
Statut:
ppublish
Résumé
Inflammatory bowel disease (IBD) is a considerable threat to human health with a significant risk for colorectal cancer (CRC). However, currently, both the molecular pathogenesis and therapeutic treatment of IBD remain limited. In this report, using both systemic and intestinal epithelium-specific gene knockout mouse models, we demonstrate that FBXO22, a substrate receptor within the SKP1-Cullin 1-F-box family of E3 ubiquitin ligases, plays an inhibitory role in the Azoxymethane
Identifiants
pubmed: 39485803
doi: 10.1073/pnas.2402035121
doi:
Substances chimiques
TOR Serine-Threonine Kinases
EC 2.7.11.1
F-Box Proteins
0
mTOR protein, mouse
EC 2.7.1.1
Azoxymethane
MO0N1J0SEN
FBXO22 protein, human
0
MTOR protein, human
EC 2.7.1.1
Dextran Sulfate
9042-14-2
Receptors, Cytoplasmic and Nuclear
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e2402035121Déclaration de conflit d'intérêts
Competing interests statement:The authors declare no competing interest.