We have studied the mechanism of apoptosis elicited by the farnesyltransferase inhibitor (R)-7-cyano-2,3,4,5-tetrahydro-1-(1H-imidazol-4-ylmethyl)-3-(phenylmethyl)-4-(2-thienylsulfonyl)-1H-1,4-benzodiazepine (BMS-214662) in human myeloma cell lines. Low concentrations of BMS-214662 efficiently inhibited protein farnesylation but did not affect the activation of Akt. BMS-214662 treatment increas...

BACKGROUND One of two proapoptotic Bcl-2 proteins, Bak or Bax, is required to permeabilize the mitochondrial outer membrane during apoptosis. While Bax is mostly cytosolic and translocates to mitochondria following an apoptotic stimulus, Bak is constitutively integrated within the outer membrane. Membrane anchorage occurs via a C-terminal transmembrane domain that has been studied in Bax but no...

Endothelial progenitor cells (EPCs) are an independent factor predicting cardiovascular events. Visfatin plays an important role in the pathogenesis of various metabolic disorders. In this study, we examined the effects of visfatin on the apoptosis of EPCs and the mechanisms underlying these effects. Cultured EPCs pre-treated with various concentrations of visfatin, FK866 (visfatin inhibitor) a...

Purpose: To investigate the influence of elemene on growth and apoptotic changes in bladder cancer cells, involvement phosphatase tensin homologous protein (PTEN)-serine/threonine kinase (Akt) signal pathway process.
 Methods: Human cell line SV-HUC-1 human T24 were randomly assigned to blank control group groups. Protein expression levels apoptosis-related factors (Bcl-2, Bax, caspase-3] ...

Prompt coronary reperfusion is the gold standard for minimizing injury following acute myocardial infarction. Rapamycin, mammalian target of Rapamycin (mTOR) inhibitor, exerts preconditioning-like cardioprotective effects against ischemia/reperfusion (I/R) injury. We hypothesized that Rapamycin, given at the onset of reperfusion, reduces myocardial infarct size through modulation of mTOR comple...

We previously showed that silencing of NbBPS1 encoding an endoplasmic reticulum (ER)-localized protein results in pleiotrophic developmental defects and cell death in Nicotiana benthamiana [Kang et al. (2008)]. In this study, we investigated the mechanism of the cell death caused by NbBPS1 silencing. Affected leaf cells exhibited morphological markers of programmed cell death (PCD) and accumula...