« Previous
Next »
Gastroenterology
Volume 137, Issue 6
, Pages 2030-2040.e5
, December 2009
Protection of Epithelial Barrier Function by the Crohn's Disease Associated Gene Protein Tyrosine Phosphatase N2
References
- . Combinatorial control of the specificity of protein tyrosine phosphatases. Curr Opin Cell Biol. 2001;13:182–195
- Replication of signals from different studies of Crohn's disease identifies previously unknown disease loci for ulcerative colitis. Nat Genet. 2008;40:713–715
- Sequence variants in the autophagy gene IRGM and multiple other replicating loci contribute to Crohn's disease susceptibility. Nat Genet. 2007;39:830–832
- Genetic determinants of ulcerative colitis include the ECM1 locus and five loci implicated in Crohn's disease. Nat Genet. 2008;40:710–712
- . Genome-wide association study of 14,000 cases of seven common diseases and 3000 shared controls. Nature. 2007;447:661–678
- Confirmation of multiple Crohn's disease susceptibility loci in a large Dutch-Belgian cohort. Am J Gastroenterol. 2009;104:630–638
- Identification of a nuclear Stat1 protein tyrosine phosphatase. Mol Cell Biol. 2002;22:5662–5668
- Cellular stress regulates the nucleocytoplasmic distribution of the protein-tyrosine phosphatase TCPTP. J Biol Chem. 2001;276:37700–37707
- Epidermal growth factor receptor and the adaptor protein p52Shc are specific substrates of T-cell protein tyrosine phosphatase. Mol Cell Biol. 1998;18:1622–1634
- Negative regulation of EGFR signalling through integrin-α1β1-mediated activation of protein tyrosine phosphatase TCPTP. Nat Cell Biol. 2005;7:78–85
- The nuclear isoform of protein-tyrosine phosphatase TC-PTP regulates interleukin-6-mediated signaling pathway through STAT3 dephosphorylation. Biochem Biophys Res Commun. 2002;297:811–817
- The T-cell protein tyrosine phosphatase. Semin Immunol. 2000;12:379–386
- Regulation of insulin receptor signaling by the protein tyrosine phosphatase TCPTP. Mol Cell Biol. 2003;23:2096–2108
- . Arginine methylation of STAT1 regulates its dephosphorylation by T-cell protein tyrosine phosphatase. J Biol Chem. 2002;277:35787–35790
- . Inflammatory bowel disease. N Engl J Med. 2002;347:417–429
- Disparate CD4+ lamina propria (LP) lymphokine secretion profiles in inflammatory bowel disease (Crohn's disease LP cells manifest increased secretion of IFN-γ, whereas ulcerative colitis LP cells manifest increased secretion of IL-5). J Immunol. 1996;157:1261–1270
- How cells respond to interferons. Annu Rev Biochem. 1998;67:227–264
- Activation pattern of signal transducers and activators of transcription (STAT) factors in inflammatory bowel diseases. Am J Gastroenterol. 2005;100:64–72
- Activation of signal transducer and activator of transcription (STAT) 1 in human chronic inflammatory bowel disease. Gut. 2002;51:379–385
- Changes in expression and distribution of claudin 2, 5, and 8 lead to discontinuous tight junctions and barrier dysfunction in active Crohn's disease. Gut. 2007;56:61–72
- Inflammatory processes have differential effects on claudins 2, 3 and 4 in colonic epithelial cells. Lab Invest. 2005;85:1139–1162
- Claudin-2 expression induces cation-selective channels in tight junctions of epithelial cells. J Cell Sci. 2002;115:4969–4976
- The density of small tight junction pores varies among cell types and is increased by expression of claudin-2. J Cell Sci. 2008;121:298–305
- Claudins regulate the intestinal barrier in response to immune mediators. Gastroenterology. 2000;118:1001–1011
- . Interferon-γ activates EGF receptor and increases TGF-α in T84 cells: implications for chloride secretion. Am J Physiol Gastrointest Liver Physiol. 2002;283:G923–G931
- The role of interferon-γ in the pathogenesis of Crohn's disease. Gastroenterol Jpn. 1992;27:29–36
- AMP-activated protein kinase mediates the interferon γ-induced decrease in intestinal epithelial barrier function. J Biol Chem. 2009;284:27952–27963
- T-cell protein tyrosine phosphatase deletion results in progressive systemic inflammatory disease. Blood. 2004;103:3457–3464
- Stat3 as an oncogene. Cell. 1999;98:295–303
- . The role of signal transducers and activators of transcription in colon cancer. Front Biosci. 2008;13:2888–2899
- AMP-activated protein kinase: an ultrasensitive system for monitoring cellular energy charge. Biochem J. 1999;338:717–722
- . Interferon-γ directly affects barrier function of cultured intestinal epithelial monolayers. J Clin Invest. 1989;83:724–727
- Inhibition of Na+, K+-ATPase by interferon-γ down-regulates intestinal epithelial transport and barrier function. Gastroenterology. 2001;120:1393–1403
- Decreased expression of apical Na+ channels and basolateral Na+, K+-ATPase in ulcerative colitis. J Pathol. 2004;204:84–92
- Altered tight junction structure contributes to the impaired epithelial barrier function in ulcerative colitis. Gastroenterology. 1999;116:301–309
- . Reversal of charge selectivity in cation or anion-selective epithelial lines by expression of different claudins. Am J Physiol Renal Physiol. 2003;285:F1078–F1084
- . Altered permeability in inflammatory bowel disease: pathophysiology and clinical implications. Curr Opin Gastroenterol. 2007;23:379–383
- . Manner of interaction of heterogeneous claudin species within and between tight junction strands. J Cell Biol. 1999;147:891–903
- Interferon-γ selectively increases epithelial permeability to large molecules by activating different populations of paracellular pores. J Cell Sci. 2005;118:5221–5230
- Cloning of the human claudin-2 5′-flanking region revealed a TATA-less promoter with conserved binding sites in mouse and human for caudal-related homeodomain proteins and hepatocyte nuclear factor-1α. J Biol Chem. 2002;277:21361–21370
- DNA binding specificity of different STAT proteins (Comparison of in vitro specificity with natural target sites). J Biol Chem. 2001;276:6675–6688
Conflicts of interest The authors disclose no conflicts.
FundingSupported by a Crohn's and Colitis Foundation of America Senior Research Award (to D.F.M.); a Jon I. Isenberg Award (to D.F.M.); grants from the German Research Foundation (DFG) (to M.S. and G.P.); NIH grant DK28305 (to K.E.B.); an unrestricted research gift from the Shape-Up Settlement fund (to K.E.B.); and by the University of California, San Diego, Digestive Diseases Research Development Center (DK080506).
PII: S0016-5085(09)01757-0
doi: 10.1053/j.gastro.2009.07.078
© 2009 AGA Institute. Published by Elsevier Inc. All rights reserved.
« Previous
Next »
Gastroenterology
Volume 137, Issue 6
, Pages 2030-2040.e5
, December 2009

