PLK-1: Angel or devil for cell cycle progression
Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, ISSN: 0304-419X, Vol: 1865, Issue: 2, Page: 190-203
2016
- 43Citations
- 58Captures
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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
- Citations43
- Citation Indexes43
- 43
- CrossRef17
- Captures58
- Readers58
- 58
Review Description
PLK-1 is a key player in the eukaryotic cell cycle. Cell cycle progression is precisely controlled by cell cycle regulatory kinases. PLK-1 is a mitotic kinase that actively regulates the G2/M transition, mitosis, mitotic exit, and cytokinesis. During cell cycle progression, PLK-1 controls various events related to the cell cycle maturation, directly and/or indirectly. On the contrary, aberrant expression of PLK-1 is strongly associated with tumorigenesis and its poor prognosis. The misexpression of PLK-1 causes the abnormalities including aneuploidy, mitotic defects, leading to tumorigenesis through inhibiting the p53 and pRB genes. Therefore, we reviewed the role of PLK-1 in the cell cycle progression and in the tumorigenesis either as a cell cycle regulator or on an attractive anti-cancer drug target.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0304419X16300191; http://dx.doi.org/10.1016/j.bbcan.2016.02.003; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84960423583&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/26899266; https://linkinghub.elsevier.com/retrieve/pii/S0304419X16300191; https://dx.doi.org/10.1016/j.bbcan.2016.02.003
Elsevier BV
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