Su, Hong-Lin <br/><br/>
Japanese encephalitis virus infection initiates endoplasmic reticulum stress and an unfolded protein response.  [electronic resource] 

 -  Journal of virology  May 2002 
 - 4162-71 p.  digital 
<br/><br/> Publication Type: Journal Article; Research Support, Non-U.S. Gov't 
<br/><br/><label>ISSN: </label>0022-538X 
<br/><br/><label>Standard No.: </label>10.1128/jvi.76.9.4162-4171.2002  doi 
<br/><br/><label>Subjects--Topical Terms: </label><br/>Animals<br/>Apoptosis<br/>CCAAT-Enhancer-Binding Proteins--metabolism<br/>Cell Line<br/>Encephalitis Virus, Japanese--pathogenicity<br/>Endoplasmic Reticulum--metabolism<br/>Gene Expression Regulation<br/>Mitogen-Activated Protein Kinases--metabolism<br/>Molecular Chaperones--metabolism<br/>Protein Folding<br/>Proto-Oncogene Proteins c-bcl-2--metabolism<br/>Transcription Factor CHOP<br/>Transcription Factors--metabolism<br/>p38 Mitogen-Activated Protein Kinases