NF-AT-Driven interleukin-4 transcription potentiated by NIP45

Science
M R HodgeL H Glimcher

Abstract

The induction of cytokine gene transcription is mediated in part by the nuclear factor of activated T cells (NF-AT). Factors involved in the mechanisms of NF-AT-mediated transcription are not well understood. A nuclear factor that interacted with the Rel homology domain (RHD) of NF-ATp was identified with the use of a two-hybrid interaction trap. Designated NIP45 (NF-AT interacting protein), it has minimal similarity to any known genes. Transcripts encoding this factor were enriched in lymphoid tissues and testes. NIP45 synergized with NF-ATp and the proto-oncogene c-Maf to activate the interleukin-4 (IL-4) cytokine promoter; transient overexpression of NIP45 with NF-ATp and c-maf in B lymphoma cells induced measurable endogenous IL-4 protein production. The identification of NIP45 advances our understanding of gene activation of cytokines, critical mediators of the immune response.

References

Jun 1, 1994·Immunity·L VenkataramanR Sen

❮ Previous
Next ❯

Citations

Feb 10, 2000·Springer Seminars in Immunopathology·J D FarrarK M Murphy
Mar 6, 2007·Pflügers Archiv : European journal of physiology·Magali SavignacJose R Naranjo
Feb 11, 2000·The Journal of Allergy and Clinical Immunology·L B Bacharier, R S Geha
Jan 17, 2002·Molecular Immunology·A F HollowayM F Shannon
Nov 9, 2000·Immunology Today·J RengarajanL H Glimcher
Jan 27, 1998·Immunobiology·M Li-WeberP H Krammer
Oct 30, 1998·Cellular Signalling·E S MasudaN Arai
May 29, 1998·Current Opinion in Immunology·K M Murphy
Aug 1, 1997·Current Opinion in Biotechnology·G Peltz
Jun 5, 2003·International Immunopharmacology·Kiyoshi Takatsu, Ai Kariyone
Apr 14, 2009·Nature Structural & Molecular Biology·John PruddenMichael N Boddy
Jan 29, 2000·Immunology·D J CousinsD Z Staynov
Oct 7, 2009·Proceedings of the National Academy of Sciences of the United States of America·Richard G JennerGraham M Lord
Feb 6, 2010·Proceedings of the National Academy of Sciences of the United States of America·John W FathmanKerri A Mowen
May 23, 1998·The Journal of Experimental Medicine·H Huang, W E Paul
Apr 17, 2002·The Journal of Experimental Medicine·Jyothi RengarajanLaurie H Glimcher
Dec 1, 1999·Inflammatory Bowel Diseases·S Romagnani
Nov 24, 1998·Allergy·S Romagnani
Aug 5, 2003·Molecular and Cellular Biology·Michael N BoddyPaul Russell
Jun 8, 1999·Annual Review of Immunology·C T Kuo, J M Leiden
Feb 28, 2002·Annual Review of Immunology·Stephen T Smale, Amanda G Fisher
Dec 23, 1998·Proceedings of the National Academy of Sciences of the United States of America·I C HoL H Glimcher
Apr 1, 1997·Proceedings of the National Academy of Sciences of the United States of America·J Hu-LiW E Paul
Dec 21, 2000·Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology·P LavenderT Lee
Jan 1, 2006·Expert Review of Clinical Immunology·Marc Williams, Steve Georas
Dec 23, 2008·Expert Review of Molecular Diagnostics·Michael Wegmann
Apr 3, 2009·Biochemical and Biophysical Research Communications·Sung Ho LeeBok Yun Kang
Apr 9, 2008·The Journal of Allergy and Clinical Immunology·Talal A ChatilaAndre E Nel
Sep 24, 2004·European Journal of Immunology·Adam F CunninghamIan C M MacLennan
Nov 18, 2004·Immunological Reviews·Kerri A Mowen, Laurie H Glimcher
Nov 23, 2011·Journal of Cellular Biochemistry·Srinivasan ShanmugarajanWilliam L Ries
Jan 16, 2010·Proteins·Naotaka SekiyamaMasahiro Shirakawa
Apr 18, 2006·Current Opinion in Immunology·Fabien BlanchetOreste Acuto
Dec 14, 2002·Immunity·Bernd ElserMin Li-Weber

❮ Previous
Next ❯

Related Concepts

Related Feeds

B-Cell Lymphoma

B-cell lymphomas include lymphomas that affect B cells. This subtype of cancer accounts for over 80% of non-Hodgkin lymphomas in the US. Here is the latest research.

Ataxia telangiectasia (MDS)

Ataxia telangiectasia is a rare neurodegenerative diseases caused by defects in the ATM gene, which is involved in DNA damage recognition and repair pathways. Here is the latest research on this autosomal recessive disease.