The Batten disease gene CLN3 confers resistance to endoplasmic reticulum stress induced by tunicamycin

Biochemical and Biophysical Research Communications

Volumn 447, Issue 1, 2014, Pages 115-120

  Wu, Dan ^a   Liu, Jing ^a   Wu, Baiyan ^a   Tu, Bo ^a   Zhu, Weiguo ^a   Luo, Jianyuan ^a,b  

^a PEKING UNIVERSITY HEALTH SCIENCE CENTER   (China)

^b UNIVERSITY OF MARYLAND SCHOOL OF MEDICINE   (United States)

Author keywords

CLN3; Endoplasmic reticulum (ER) stress; JNCL; Tunicamycin

Indexed keywords

CCAAT ENHANCER BINDING PROTEIN; CHAPERONE; GLUCOSE REGULATED PROTEIN 78; SMALL INTERFERING RNA; TUNICAMYCIN;

APOPTOSIS; ARTICLE; CELL FUNCTION; CELL PROLIFERATION; CLN3 GENE; DNA TRANSFECTION; ENDOPLASMIC RETICULUM STRESS; GENE; GENE FUNCTION; HUMAN; HUMAN CELL; MUTANT; NERVE CELL DEGENERATION; NEURONAL CEROID LIPOFUSCINOSIS; PRIORITY JOURNAL; WILD TYPE;

CLN3; ENDOPLASMIC RETICULUM (ER) STRESS; JNCL; TUNICAMYCIN;

APOPTOSIS; CELL LINE, TUMOR; CELL PROLIFERATION; ENDOPLASMIC RETICULUM STRESS; HEAT-SHOCK PROTEINS; HUMANS; MEMBRANE GLYCOPROTEINS; MOLECULAR CHAPERONES; NEURONAL CEROID-LIPOFUSCINOSES; TRANSCRIPTION FACTOR CHOP; TUNICAMYCIN;

EID: 84899477384     PISSN: 0006291X     EISSN: 10902104     Source Type: Journal    
DOI: 10.1016/j.bbrc.2014.03.120     Document Type: Article

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