The role of sumoylation in senescence
SUMO Regulation of Cellular Processes, Page: 201-216
2009
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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.
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Book Chapter Description
Cellular senescence is a program initiated by many stress signals including aberrant activation of oncogenes, DNA damage, oxidative lesions and telomere attrition. Once engaged senescence irreversibly limits cellular proliferation and potently prevents tumor formation in vivo. The precise mechanisms driving the onset of senescence are still not completely defined, although the pRb and p53 tumor suppressor pathways converge with the SUMO cascade to regulate cellular senescence. Sumoylation translocates p53 to PML nuclear bodies where it can co-operate with many sumoylated co-factors in a program that activates pRb and favors senescence. Once activated pRb integrates various proteins, many of them sumoylated, into a repressor complex that inhibits the transcription of proliferation-promoting genes and initiates chromatin condensation. Sumoylation is required for heterochromatin formation during senescence and may act as a scaffold to stabilize the pRb repressor complex. Thus, SUMO is a critical component of a tumor-suppressor network that limits aberrant cell proliferation and tumorigenesis. © Springer Science+Business Media B.V. 2009.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84901127385&origin=inward; http://dx.doi.org/10.1007/978-90-481-2649-1_12; http://link.springer.com/10.1007/978-90-481-2649-1_12; http://www.springerlink.com/index/10.1007/978-90-481-2649-1_12; http://www.springerlink.com/index/pdf/10.1007/978-90-481-2649-1_12; https://link.springer.com/chapter/10.1007%2F978-90-481-2649-1_12
Springer Science and Business Media LLC
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