| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
J Biol Chem, Vol. 275, Issue 16, 12313-12320, April 21, 2000
From the The HCMV IE2 protein negatively autoregulates its
own expression as well as represses the transactivation activity of
p53. Using the repression domain of IE2 as bait in the yeast two-hybrid system, Nrf1 and Nrf2, members of the CNC-bZIP family, were
found to be IE2-interacting proteins. Residues 331-448 encompassing the DNA-binding and the dimerization domains of Nrf1 are sufficient for
the interaction. The interaction was further confirmed in vitro by a glutathione S-transferase pull-down assay
and in vivo by co-immunoprecipitation. In transient
transfection studies, transcription driven by six copies of an NF-E2
site or by chimeric proteins between the DNA-binding domain of LexA and
members of the CNC-bZIP family is repressed by IE2. Importantly, the
DNA binding activity of the Nrf1/MafK heterodimer is not impeded by IE2. In a parallel study, CNC-bZIP factors attenuate the negative autoregulation of IE2. The attenuation could be explained by the finding that Nrf1 functions alone and synergistically with its heterodimerization partner, MafK, in inhibiting the DNA binding activity of IE2. Taken together, these results demonstrate the existence of antagonism between members of the CNC-bZIP family and IE2.
Antagonism between Members of the CNC-bZIP Family and the
Immediate-Early Protein IE2 of Human Cytomegalovirus*
§¶,§¶,,,
, and
Institute of Biomedical Sciences, Academia
Sinica, Taipei 115, Taiwan and the § Graduate Institute of
Life Sciences, National Defense Medical Center,
Taipei 100, Taiwan
*
This work was supported by grants from the Academia Sinica
and the National Science Council of Taiwan (to C. W. W. and
Y. S. L.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed. Tel.:
886-2-26523074; Fax: 886-2-27829142; E-mail:
bmyslin@ccvax.sinica.edu.tw.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  C.J. Carter Schizophrenia Susceptibility Genes Directly Implicated in the Life Cycles of Pathogens: Cytomegalovirus, Influenza, Herpes simplex, Rubella, and Toxoplasma gondii Schizophr Bull, June 13, 2008; (2008) sbn054v1. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S.-K. Wang, C.-Y. Duh, and C.-W. Wu Human Cytomegalovirus UL76 Encodes a Novel Virion-Associated Protein That Is Able To Inhibit Viral Replication J. Virol., September 15, 2004; 78(18): 9750 - 9762. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C.-Y. Wang, Y.-J. Liang, Y.-S. Lin, H.-M. Shih, Y.-S. Jou, and W. C. Y. Yu YY1AP, A Novel Co-activator of YY1 J. Biol. Chem., April 23, 2004; 279(17): 17750 - 17755. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. Sanchez, C. L. Clark, J. Y. Yen, R. Dwarakanath, and D. H. Spector Viable Human Cytomegalovirus Recombinant Virus with an Internal Deletion of the IE2 86 Gene Affects Late Stages of Viral Replication J. Virol., February 22, 2002; 76(6): 2973 - 2989. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |
