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Cdc25

About: Cdc25 is a research topic. Over the lifetime, 727 publications have been published within this topic receiving 58224 citations. The topic is also known as: Cdc25 phosphatase.


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Journal ArticleDOI
TL;DR: A speculative model where binding of 14‐3‐3 to multiple sites on some ligands results in global ligand conformational changes that mediate their biological effects is presented and may prove to be a bona fide phosphodependent signaling chaperone.

656 citations

Journal ArticleDOI
TL;DR: The roles of CDC25 phosphatases in both normal and abnormal cell proliferation are focused on, a critical assessment of the current data on CDC25 overexpression in cancer is provided, and both current and future therapeutic strategies for targeting CDC25 activity in cancer treatment are discussed.
Abstract: Cell division cycle 25 (CDC25) phosphatases regulate key transitions between cell cycle phases during normal cell division, and in the event of DNA damage they are key targets of the checkpoint machinery that ensures genetic stability. Taking only this into consideration, it is not surprising that CDC25 overexpression has been reported in a significant number of human cancers. However, in light of the significant body of evidence detailing the stringent complexity with which CDC25 activities are regulated, the significance of CDC25 overexpression in a subset of cancers and its association with poor prognosis are proving difficult to assess. We will focus on the roles of CDC25 phosphatases in both normal and abnormal cell proliferation, provide a critical assessment of the current data on CDC25 overexpression in cancer, and discuss both current and future therapeutic strategies for targeting CDC25 activity in cancer treatment.

655 citations

Journal ArticleDOI
04 Oct 1991-Cell
TL;DR: The cdc25-dependent cleavage reaction closely resembles dephosphorylation by known tyrosine phosphatases: the reaction requires a reducing agent, shows high sensitivity to sodium vanadate, and proceeds efficiently in the presence of metal chelators.

574 citations

Journal ArticleDOI
TL;DR: The cell cycle is a complex process that involves numerous regulatory proteins that direct the cell through a specific sequence of events culminating in mitosis and the production of two daughter cells, and should be considered in the design of studies using such chemicals.
Abstract: The cell cycle is a complex process that involves numerous regulatory proteins that direct the cell through a specific sequence of events culminating in mitosis and the production of two daughter cells. Central to this process are the cyclin-dependent kinases (cdks), which complex with the cyclin proteins. These proteins regulate the cell's progression through the stages of the cell cycle and are in turn regulated by numerous proteins, including p53, p21, p16, and cdc25. Downstream targets of cyclin-cdk complexes include pRb and E2F. The cell cycle can be altered to the advantage of many viral agents, most notably polyomaviruses, papillomaviruses, and adenoviruses. The cell cycle often is dysregulated in neoplasia due to alterations either in oncogenes that indirectly affect the cell cycle or in tumor suppressor genes or oncogenes that directly impact cell cycle regulation, such as pRb, p53, p16, cyclin D1, or mdm-2. The cell cycle has become an intense subject of research in recent years. This research has led to the development of techniques useful for the determination of the effects of drugs and toxins on the cell cycle. Any drug or toxin with DNA damaging ability would be expected to alter cell cycle progression, and therefore, the cell cycle should be considered in the design of studies using such chemicals. With the appropriate techniques, cell cycle alterations may also be detected in tissue sections. Because of the ubiquitous nature of the cell cycle, it deserves consideration in the design and interpretation of studies in a wide variety of disciplines.

560 citations

Journal ArticleDOI
06 Sep 1996-Science
TL;DR: Plx1, a kinase that associates with and phosphorylates the amino-terminal domain of Cdc25, was purified extensively from Xenopus egg extracts and revealed that it is related to the Polo family of protein kinases, which indicates that Plx1 may participate in control of mitotic progression.
Abstract: Cdc2, the cyclin-dependent kinase that controls mitosis, is negatively regulated by phosphorylation on its threonine-14 and tyrosine-15 residues. Cdc25, the phosphatase that dephosphorylates both of these residues, undergoes activation and phosphorylation by multiple kinases at mitosis. Plx1, a kinase that associates with and phosphorylates the amino-terminal domain of Cdc25, was purified extensively from Xenopus egg extracts. Cloning of its complementary DNA revealed that Plx1 is related to the Polo family of protein kinases. Recombinant Plx1 phosphorylated Cdc25 and stimulated its activity in a purified system. Cdc25 phosphorylated by Plx1 reacted strongly with MPM-2, a monoclonal antibody to mitotic phosphoproteins. These studies indicate that Plx1 may participate in control of mitotic progression.

536 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202310
202217
20219
20209
201912
20189