Death squads enlisted by the tumour suppressor p53
Biochemical and Biophysical Research Communications, ISSN: 0006-291X, Vol: 331, Issue: 3, Page: 786-798
2005
- 105Citations
- 44Captures
Metric Options: CountsSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations105
- Citation Indexes104
- 104
- CrossRef88
- Patent Family Citations1
- Patent Families1
- Captures44
- Readers44
- 44
Review Description
p53 is a tumour suppressor that is found mutated or functionally inactivated in more than half of all human cancers. p53 function is activated by DNA damage, hypoxia, expression of certain oncogenes, and many cytotoxic stimuli. p53 is a transcription factor that regulates expression of target genes which promote apoptotic cell death, cell cycle arrest, cellular senescence, and some other processes. In this review we summarise current knowledge of p53 target genes implicated in apoptosis signalling.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0006291X05007060; http://dx.doi.org/10.1016/j.bbrc.2005.03.183; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=18144364007&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/15865934; https://linkinghub.elsevier.com/retrieve/pii/S0006291X05007060; https://dx.doi.org/10.1016/j.bbrc.2005.03.183
Elsevier BV
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