Role of BAX in the apoptotic response to anticancer agents.

By Lin Zhang, Jian Yu, B. Park, Kenneth W. Kinzler, Bert Vogelstein. Science, 2000

947 citations recorded by the source corpus.

Subfields: Biotechnology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/e98210221fd19dcd6d6e4fc7196b3bad2c130144

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Citations in the corpus

Smac agonists sensitize for Apo2L/TRAIL- or anticancer drug-induced apoptosis and induce regression of malignant glioma in vivo (2002, background): “However, TRAIL may not be effective in tumors with defects in activation of the mitochondrial pathway due to high expression of Bcl-2, BAX mutations or Apaf1 inactivatio”
Colorectal cancer prevention and treatment by inhibition of cyclooxygenase-2 (2001, background): “cgi?l=581"> BAX in NSAID-induced colorectal-cancer-cell apoptosis has been indicate”
The Bcl2 family: regulators of the cellular life-or-death switch (2002, background): “Moreover, elimination of Bax from human colorectal cancer cells abolished their apoptotic response to non-steroidal anti-inflammatory drug”
Control of apoptosis by p53 (2003, background): “Moreover, disruption of either Bax or Puma in HCT116 cells Oncogene produces various degrees of apoptotic defects (Zhang et al., 2000; Yu et al., 2003).”
Acetylation of the p53 DNA-binding domain regulates apoptosis induction. (2006, background): “In human cells, p53 requires both BAX and PUMA to efficiently induce apoptosis (Chipuk et al., 2003; Jeffers et al., 2003; Villunger et al., 2003; Yu et al., 2003; Zhang et al., 2000).”
Apoptosis A Link between Cancer Genetics and Chemotherapy (2002, background): “In Zhang et al., 2000), and are associated with multidrugsolid tumors and non-T cell leukemias, tumor surveilresistance in human cancers (Reed, 1999).”
BH3-only proteins that bind pro-survival Bcl-2 family members fail to induce apoptosis in the absence of Bax and Bak. (2001, background): “To a lesser extent, Bax mutation has been implicated in human leukemias, gastrointestinal cancer, and colorectal cancer (Rampino et al. 1997; Zhang et al. 2000).”
Humanin peptide suppresses apoptosis by interfering with Bax activation (2003, background): “Vogelstein) in which the remaining allele was disrupted by homologous recombination, producing Bax-deficient cell”
Linking of autophagy to ubiquitin-proteasome system is important for the regulation of endoplasmic reticulum stress and cell viability. (2007, background): “more sensitive pro-death molecule Bax but not the less sensitive pro-death molecule Bak, which is expressed in the Bax-deficient HCT 116.(14,48) A previous study had shown that apoptosis could be induced in Bax-deficient but Bak-positive HCT 116 cells with stronger death stimulations.”
5-Fluorouracil: mechanisms of action and clinical strategies (2003, positive): “It has been shown that disrupting both alleles of TP53 or BAX in a colon cancer cell line made the cells strikingly resistant to apoptosis induced by 5-FU compared with the parental lin”
The Bcl-2 family: roles in cell survival and oncogenesis (2003, background): “Other evidence also suggests that the functions of Bax and Bak may not be entirely equivalent (Zhang et al., 2000; Gillissen et al., 2003).”
Molecular mechanisms of drug resistance (2005, background): “It has also been demonstrated that downregulating Bcl-2 and Bcl-XL using antisense techniques sensitizes cells to chemotherapy [137,158,160], whereas loss of Bax expression has been found to decrease chemosensitivity [161].”
Apoptosis-based therapies (2002, background): “NSAIDs have also been reported to reduce BCLXL expression and induce apoptosis of colon cancer cells in vitro through a BAX-dependent mechanis”
Apoptosis defects and chemotherapy resistance: molecular interaction maps and networks (2004, background): “…& 2004 Nature Publishing Group All rights reserved 0950-9232/04 $25.00 www.nature.com/onc cells are resistant to mitochondria-mediated apoptosis (Zhang et al., 2000; Schmitt and Lowe, 2002), and overexpression of exogenous Bcl-xL or Bcl-2 suppresses apoptosis (Schott et al., 1995; Walczak et…”