Open AccessNOX1 Regulates Collective and Planktonic Cell Migration: Insights From Patients With Pediatric-Onset IBD and NOX1 Deficiency
Author(s) -
Razieh Khoshnevisan,
Michael J. Anderson,
Stephen Babcock,
Sierra Anderson,
David W. Illig,
Benjamin Marquardt,
Roya Sherkat,
Katrin Schröder,
Franziska Moll,
Sebastian Hollizeck,
Meino Rohlfs,
Christoph Walz,
Peyman Adibi,
Abbas Rezaei,
Alireza Andalib,
Sibylle Koletzko,
Aleixo M. Muise,
Scott B. Snapper,
Christoph Klein,
Jay R. Thiagarajah,
Daniel Kotlarz
Publication year - 2020
Publication title -
inflammatory bowel diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.932
H-Index - 146
eISSN - 1536-4844
pISSN - 1078-0998
DOI - 10.1093/ibd/izaa017
Subject(s) - cell migration , nox1 , wound healing , biology , microbiology and biotechnology , medicine , cancer research , immunology , cell , genetics , reactive oxygen species , nadph oxidase
Genetic defects of pediatric-onset inflammatory bowel disease (IBD) provide critical insights into molecular factors controlling intestinal homeostasis. NOX1 has been recently recognized as a major source of reactive oxygen species (ROS) in human colonic epithelial cells. Here we assessed the functional consequences of human NOX1 deficiency with respect to wound healing and epithelial migration by studying pediatric IBD patients presenting with a stop-gain mutation in NOX1.