The JI
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     
 


This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Data Supplement
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Klamp, T.
Right arrow Articles by Howard, J. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Klamp, T.
Right arrow Articles by Howard, J. C.
The Journal of Immunology, 2003, 171: 1255-1265.
Copyright © 2003 by The American Association of Immunologists

A Giant GTPase, Very Large Inducible GTPase-1, Is Inducible by IFNs 1

Thorsten Klamp*, Ulrich Boehm2,*, Daniela Schenk*, Klaus Pfeffer{dagger} and Jonathan C. Howard3,*

* Institute for Genetics, University of Cologne, Cologne, Germany; and {dagger} Institute for Medical Microbiology, University of Düsseldorf, Düsseldorf, Germany

The complex, partially overlapping, cellular responses to IFN type I (IFN-{alpha} and -{beta}) and IFN type II (IFN-{gamma}) involve several hundred genes that can be largely classified in terms of specific cellular programs functional in innate and adaptive immunity. Among these programs are previously unconsidered mechanisms of cell-autonomous resistance against various pathogens mediated by dedicated, largely novel families of GTPases. We report here the identification and characterization of a new GTPase family that contributes to the cellular response to both type I and type II IFNs. We name this family the very large inducible GTPases (VLIGs). The prototype VLIG, VLIG-1, is a strongly IFN-inducible, soluble, cytosolic and nuclear protein of 280 kDa. The open reading frame of VLIG-1 is encoded on a single very large exon, and outside the canonical GTP-binding motifs, sequence and structural prediction suggest a unique family without significant relationship to other known protein families. Within the GTPase superfamily the VLIG family is more closely related to IFN-inducible GTPases mediating cell-autonomous resistance than to other GTPase families. In addition, we provide evidence that VLIG-1 is polymorphic in mice of different genetic backgrounds and is a member of a small gene family on mouse chromosome 7 with a conserved homologue located on human chromosome 11.




This article has been cited by other articles:


Home page
Mol Biol EvolHome page
G. Li, J. Zhang, Y. Sun, H. Wang, and Y. Wang
The Evolutionarily Dynamic IFN-Inducible GTPase Proteins Play Conserved Immune Functions in Vertebrates and Cephalochordates
Mol. Biol. Evol., July 1, 2009; 26(7): 1619 - 1630.
[Abstract] [Full Text] [PDF]


Home page
Physiol. GenomicsHome page
C. J. Krebs, S. Khan, J. W. MacDonald, M. Sorenson, and D. M. Robins
Regulator of sex-limitation KRAB zinc finger proteins modulate sex-dependent and -independent liver metabolism
Physiol Genomics, June 1, 2009; 38(1): 16 - 28.
[Abstract] [Full Text] [PDF]


Home page
Mol. Cell. Biol.Home page
A. Dufner, G. S. Duncan, A. Wakeham, A. R. Elford, H. T. Hall, P. S. Ohashi, and T. W. Mak
CARD6 Is Interferon Inducible but Not Involved in Nucleotide-Binding Oligomerization Domain Protein Signaling Leading to NF-{kappa}B Activation
Mol. Cell. Biol., March 1, 2008; 28(5): 1541 - 1552.
[Abstract] [Full Text] [PDF]


Home page
Sci SignalHome page
J. Colicelli
Human RAS Superfamily Proteins and Related GTPases
Sci. Signal., September 14, 2004; 2004(250): re13 - re13.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 2003 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 2003 by The American Association of Immunologists, Inc. All rights reserved.