PUMA mediates the apoptotic response to p53 in colorectal cancer cells
By Jian Yu, Zhenghe Wang, Kenneth W. Kinzler, Bert Vogelstein, Lin Zhang. Proceedings of the National Academy of Sciences of the United States of America, 2003
617 citations recorded by the source corpus.
Subfields: Biotechnology, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/ad0af2128f83b7ba014f8cf0f577de15ba509fd5
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Citations in the corpus
- The Bcl-2 family: roles in cell survival and oncogenesis (2003, background): “Indeed, multiple gene-targeting in a human colorectal cell line has recently demonstrated that Puma is required for apoptosis induced by p53 in p21 / cells (Yu et al., 2003).”
- Targeting Apoptosis Pathways in Cancer Therapy (2005, background): “The mechanism by which p53 promotes apoptosis is still not fully understood.(23,24)”
- Tip60-dependent acetylation of p53 modulates the decision between cell-cycle arrest and apoptosis. (2006, background): “The importance of PUMA is underscored by the recent observation that puma null human cells are resistant to stress-induced apoptosis ( Yu et al., 2003 ) and that puma-knockout mice recapitulate several key apoptotic deficiencies observed in p53-knockout mice (Jeffers et al., 2003; Villunger et al., ”
- Cell Death Signaling. (2015, background): “Both are direct transcriptional targets of the tumor suppressor p53 (Oda et al. 2000; Nakano and Vousden 2001; Yu et al. 2003), although other stimuli regulate their expression levels (see Table 1).”
- Apoptosis as anticancer mechanism: function and dysfunction of its modulators and targeted therapeutic strategies (2016, background): “PUMA gene is extremely effective in inducing apoptotic cell death within few hours and, more importantly, knockout experiments in human colorectal cancer cells showed that PUMA is required for p53-induced apoptosis [123].”
- 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).”
- Neuronal Cell Death. (2018, neutral): “Open questions regarding the de-inhibition model remain however, such as the observations that mitochondrial localization plays an important role in the activation of Bax by Puma, Bim, and tBid (431, 719, 728, 778).”
- Bcl-2 family proteins and cancer (2008, background): “Among the direct targets of the p53 transcription factor are BAX, BID, PUMA and NOXA (Miyashita et al., 1994; Miyashita and Reed, 1995; Oda et al., 2000; Sax et al., 2002; Yu et al., 2003), thus demonstrating strong connections between genome surveillance by p53 and cell death genes of the BCL-2 fam”