Topic
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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TL;DR: The experiments demonstrate the existence of a cDC25 regulatory system consisting of both a stimulatory kinase that phosphorylates a putative regulatory domain of the cdc25 protein and an inhibitory serine/threonine phosphatase that counteracts this kinase activity.
429 citations
TL;DR: A correlation of PTP structure and function from mutagenesis experiments is summarized and a powerful strategy is presented for creating specific and high-affinity bidentate PTP inhibitors that simultaneously bind both the active site and a unique adjacent site.
Abstract: Protein tyrosine phosphatases (PTPs) are signaling enzymes that control a diverse array of cellular processes. Malfunction of PTP activity is associated with a number of human disorders. Recent genetic and biochemical studies indicate that PTPs represent a novel platform for drug discovery. Detailed knowledge of PTP substrate specificity and the wealth of structural data on PTPs provide a solid foundation for rational PTP inhibitor design. This review summarizes a correlation of PTP structure and function from mutagenesis experiments. The molecular basis for PTP1B and MKP3 substrate recognition is discussed. A powerful strategy is presented for creating specific and high-affinity bidentate PTP inhibitors that simultaneously bind both the active site and a unique adjacent site. Finally, recent advances in the development of potent and selective inhibitors for PTP1B and Cdc25 are described.
425 citations
TL;DR: A growing family of kinases and phosphatases controls the activity of the cyclin-dependent kinase cdc2, and it is likely that other regulatory mechanisms cooperate with the wee1/cdc25 phosphorylation systems to control the action of cDC2.
423 citations
TL;DR: It is proposed that MAPKAP kinase-2 is a new member of the DNA damage checkpoint kinase family that functions in parallel with Chk1 and Chk2 to integrate DNA damage signaling responses and cell cycle arrest in mammalian cells.
422 citations
TL;DR: Recent data demonstrate that in addition to the ATM/ATR-CHK pathway, a p38-MAPKAP pathway is also involved in controlling CDC25 activity during G(2)/M checkpoint activation and highlight the significance of developing specific CDC25 inhibitors for cancer therapy.
421 citations