Редактирование: PLK1 (раздел)

==Publications==

{{medline-entry
|title=Dynactin pathway-related gene expression is altered by aging, but not by vitrification.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31260804
|abstract=The storage of surplus oocytes by cryopreservation (OC) is a widely used tool in assisted reproductive technology, but there is a great debate about the effects of cryopreservation on oocyte competence. It is known that OC may affect meiotic spindles but remains unclear if OC may increase the risk of aneuploidy. The aim of this study was to test the effects of OC and women aging on the expression of cytokinesis-related genes playing an important role in the segregation of chromosomes (DCTN1, [[DCTN2]], [[DCTN3]], [[DCTN6]] and [[PLK1]]). Results highlighted that OC do not modify the expression of the selected genes, whereas women aging modulate the expression of all transcripts, confirming that aging is the crucial factor affecting meiosis and aneuploidy risk. A new role for Dynactin and [[PLK1]] was shed in light, providing information on the ageing process in the oocyte which may be associated to reduced fertility.
|mesh-terms=* Adult
* Age Factors
* Aging
* Aneuploidy
* Cryopreservation
* Dynactin Complex
* Gene Expression
* Gene Expression Regulation
* Humans
* Oocyte Retrieval
* Oocytes
* Real-Time Polymerase Chain Reaction
* Reproductive Techniques, Assisted
* Vitrification
|keywords=* Aging
* Aneuploidy
* Cryopreservation
* Dynactin
* Gene expression
* Oocyte
|full-text-url=https://sci-hub.do/10.1016/j.reprotox.2019.06.011
}}
{{medline-entry
|title=Downregulation of Polo-like kinase 1 induces cellular senescence in human primary cells through a p53-dependent pathway.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23525475
|abstract=Polo-like kinase 1 ([[PLK1]]) plays a key role in various stages of mitosis from entry into M phase to exit from mitosis. However, its role in cellular senescence remains to be determined. Therefore, the effects of [[PLK1]] on cellular senescence in human primary cells were investigated. We found that expression of [[PLK1]] decreased in human dermal fibroblasts and human umbilical vein endothelial cells under replicative senescence and premature senescence induced by adriamycin. [[PLK1]] knockdown with [[PLK1]] small interfering RNAs in young cells induced premature senescence. In contrast, upregulation of [[PLK1]] in old cells partially reversed senescence phenotypes. Cellular senescence by [[PLK1]] inhibition was observed in p16 knockdown cells but not in p53 knockdown cells. Our data suggest that [[PLK1]] repression might result in cellular senescence in human primary cells via a p53-dependent pathway. 
|mesh-terms=* Cell Cycle Proteins
* Cells, Cultured
* Cellular Senescence
* Cyclin-Dependent Kinase Inhibitor p16
* Down-Regulation
* Gene Knockdown Techniques
* Genes, p16
* Genes, p53
* Human Umbilical Vein Endothelial Cells
* Humans
* Protein-Serine-Threonine Kinases
* Proto-Oncogene Proteins
* RNA, Messenger
* RNA, Small Interfering
* Signal Transduction
* Tumor Suppressor Protein p53
|keywords=* Cellular senescence
* Human primary cells.
* Polo-like kinase 1
* p53
|full-text-url=https://sci-hub.do/10.1093/gerona/glt017
}}