Journal
BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY
Volume 72, Issue 11, Pages 3034-3037Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1271/bbb.80422
Keywords
(-)-epigallocatechin-3-gallate (EGCG); extracellular signal-regulated protein kinase (ERK); C-jun N-terminal kinase (JNK); apoptosis; Jurkat cells
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(-)-Epigallocatechin-3-gallate (EGCG)-induced apoptosis was along both the extracellular signal-regulated protein kinase (ERK) and c-jun N-terminal kinase (JNK) pathways in Jurkat cells. Co-treatment with EGCG potentiated the cytotoxicity induced by benzyl isothiocyanate (BITC) and H2O2, both being inhibited by ERK and JNK inhibitors. These results suggest the significant role of mitogen-activated protein kinase (MAPK) signaling in the apoptosis induction regulated by EGCG alone and in combination.
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