TNFR2 activates MLCK-dependent tight junction dysregulation to cause apoptosis-mediated barrier loss and experimental colitis.
Gastroenterology
; 145(2): 407-15, 2013 Aug.
Article
in En
| MEDLINE
| ID: mdl-23619146
Key words
CA-MLCK; DSS; Disease Progression; Epithelial Barrier; IBD; Inflammatory Bowel Disease; Intestinal Permeability; MLC; MLCK; Rag1; TNF; TNFR; constitutively active myosin light chain kinase; dextran sulfate sodium; inflammatory bowel disease; myosin II regulatory light chain; myosin light chain kinase; recombinase activating gene 1; tumor necrosis factor; tumor necrosis factor receptor
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Myosin-Light-Chain Kinase
/
Colitis
/
Tight Junctions
/
Receptors, Tumor Necrosis Factor, Type I
/
Receptors, Tumor Necrosis Factor, Type II
/
Epithelial Cells
/
Intestinal Mucosa
Type of study:
Prognostic_studies
Limits:
Animals
Language:
En
Journal:
Gastroenterology
Year:
2013
Type:
Article
Affiliation country:
China