Disturbance of Copper Homeostasis Is a Mechanism for Homocysteine-Induced Vascular Endothelial Cell Injury

PLoS ONE

Volumn 8, Issue 10, 2013, Pages

  Dong, Daoyin ^a   Wang, Biao ^a   Yin, Wen ^a   Ding, Xueqing ^a   Yu, Jingjing ^b   Kang, Y James ^a  

^a SICHUAN UNIVERSITY   (China)

^b AGILENT TECHNOLOGIES   (China)

Author keywords

[No Author keywords available]

Indexed keywords

CHAPERONE; COX17 PROTEIN; CYTOCHROME C OXIDASE; HOMOCYSTEINE; UNCLASSIFIED DRUG;

ARTICLE; CELL DAMAGE; CELL DEATH; CELL VIABILITY; CELLULAR DISTRIBUTION; COMPLEX FORMATION; CONCENTRATION RESPONSE; CONTROLLED STUDY; COPPER HOMEOSTASIS; COPPER METABOLISM; ENDOTHELIUM CELL; ENZYME ACTIVITY; HIGH PERFORMANCE LIQUID CHROMATOGRAPHY; HUMAN; HUMAN CELL; IN VITRO STUDY; MASS SPECTROMETRY; MITOCHONDRIAL MEMBRANE POTENTIAL; MOLECULAR WEIGHT; PROTEIN BLOOD LEVEL; PROTEIN CONTENT; UMBILICAL VEIN ENDOTHELIAL CELL;

CARRIER PROTEINS; CELL SURVIVAL; COPPER; ELECTRON TRANSPORT COMPLEX IV; ENDOTHELIAL CELLS; HOMEOSTASIS; HOMOCYSTEINE; HUMAN UMBILICAL VEIN ENDOTHELIAL CELLS; HUMANS; INTRACELLULAR SPACE; MEMBRANE POTENTIAL, MITOCHONDRIAL; MITOCHONDRIA; NECROSIS;

EID: 84885767233     PISSN: None     EISSN: 19326203     Source Type: Journal    
DOI: 10.1371/journal.pone.0076209     Document Type: Article

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