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Isoorientin induces apoptosis through mitochondrial dysfunction and inhibition of PI3K/Akt signaling pathway in HepG2 cancer cells

Author
LI YUAN1 ; JING WANG1 ; HAIFANG XIAO1 ; CHUNXIA XIAO1 ; YUTANG WANG1 ; XUEBO LIU1
[1] Laboratory of Nutrition and Functional Factors, College of Food Science and Engineering, Northwest A & F University, Yangling, China
Source

Toxicology and applied pharmacology. 2012, Vol 265, Num 1, pp 83-92, 10 p ; ref : 3/4 p

CODEN
TXAPA9
ISSN
0041-008X
Scientific domain
Pharmacology drugs; Toxicology
Publisher
Elsevier, Amsterdam
Publication country
Netherlands
Document type
Article
Language
English
Author keyword
Apoptosis Isoorientin Mitochondrial stress NO PI3K/Akt ROS
Keyword (fr)
1-Phosphatidylinositol 3-kinase Akt protein kinase Apoptose Cellule tumorale In vitro Inhibiteur Inhibition Mitochondrie Mort cellulaire Stress Transduction signal Trouble fonctionnel Lignée HEPG2 Voie de signalisation Appareil digestif Enzyme Foie Homme Hépatocyte Lignée cellulaire Transferases
Keyword (en)
1-Phosphatidylinositol 3-kinase Akt protein kinase Apoptosis Tumor cell In vitro Inhibitor Inhibition Mitochondria Cell death Stress Signal transduction Dysfunction Signaling pathway Digestive system Enzyme Liver Human Hepatocyte Cell line Transferases
Keyword (es)
1-Phosphatidylinositol 3-kinase Akt protein kinase Apoptosis Célula tumoral In vitro Inhibidor Inhibición Mitocondria Muerte celular Estrés Transducción señal Trastorno funcional Vía de señalización Aparato digestivo Enzima Hígado Hombre Hepatocito Línea celular Transferases
Classification
Pascal
002 Biological and medical sciences / 002B Medical sciences / 002B03 Toxicology

Discipline
Toxicology
Origin
Inist-CNRS
Database
PASCAL
INIST identifier
26679936

Sauf mention contraire ci-dessus, le contenu de cette notice bibliographique peut être utilisé dans le cadre d’une licence CC BY 4.0 Inist-CNRS / Unless otherwise stated above, the content of this bibliographic record may be used under a CC BY 4.0 licence by Inist-CNRS / A menos que se haya señalado antes, el contenido de este registro bibliográfico puede ser utilizado al amparo de una licencia CC BY 4.0 Inist-CNRS

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