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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 Article
TL;DR: In this article, it was shown that the timing of mitosis is sensitive to the level of cdc25+ expression and that the cellular concentration of p80cdc25 increases as cells approach mitosis.
Abstract: In this paper, we have described the critical experiments leading to the discovery and analysis of the cdc25 M-phase inducer. We have shown that timing of mitosis is sensitive to the level of cdc25+ expression and that the cellular concentration of p80cdc25 increases as cells approach mitosis. From these observations we conclude that, in S. pombe, rate of accumulation of p80cdc25 plays an important role in determining the timing of mitosis. We postulate that under a given set of conditions, a critical level of p80cdc25 activity is required to undergo mitosis. The actual level that is required can vary depending on ploidy, growth rate, nutritional status of the cell, and perhaps other parameters. These signals may be monitored through the weel pathway leading to tyrosyl phosphorylation of p34cdc2. We have shown that p80cdc25 encodes a phosphate that acts by directly dephosphorylating the Tyr-15 residue of p34cdc2. Our studies strongly indicate that this aspect of the mitotic control network is generally conserved among eukaryotes. It is conceivable, however, that the mode of regulation of cdc25 activity may vary from species to species. Clearly, in S. cerevisiae the cdc25+ homolog, MIH1, in contrast to cdc25+, is not rate-limiting for M-phase onset. It will be important to determine whether the level of cdc25+ homologs in other organisms also oscillates during the cell cycle, or whether their activity is controlled by localization or posttranslational mechanisms, such as phosphorylation. Furthermore, our finding of more than one cdc25+ homolog in a single species suggests an additional level of complexity to the control of M-phase onset by cdc25 in higher eukaryotes that will require further investigation.
01 Jan 2011
TL;DR: The extent to which the G2/M transition is phosphoregulated by WEE1 kinase and CDC25 phosphatase, as exemplified in yeasts and animals, is discussed together with an alternative model that excludes these proteins from this transition.
Abstract: †Background The complex events of mitosis rely on precise timing and on immaculate preparation for their success, but the G2/M transition in the plant cell cycle is currently steeped in controversy and alternative models. †Scope In this brief review, the regulation of the G2/M transition in plants is commented on. The extent to which the G2/M transition is phosphoregulated by WEE1 kinase and CDC25 phosphatase, as exemplified in yeasts and animals, is discussed together with an alternative model that excludes these proteins from this transition. Arabidopsis T-DNA insertional lines for WEE1 and CDC25 that develop normally prompted the latter model. An argument is then presented that environmental stress is the norm for higher plants in temperate conditions. If so, the repressive role that WEE1 has under checkpoint conditions might be part of the normal cell cycle for many proliferative plant cells. Arabidopsis CDC25 can function as either a phosphatase or an arsenate reductase and recent evidence suggests that cdc25 knockouts are hypersensitive to hydroxyurea, a drug that induces the DNA-replication checkpoint. That other data show a null response of these knockouts to hydroxyurea leads to an airing of the controversy surrounding the enigmatic plant CDC25 at the G2/M transition.
Book ChapterDOI
01 Jan 2010
TL;DR: Recent data are discussed that define the roles of 14-3-3 in DNA-damage checkpoint pathway, which coordinate with DNA damage response regulators such as p53 and CDC25 to regulate the cell cycle to promote DNA repair or survival.
Abstract: DNA damage causes cell cycle delay, and this process involves a number of highly-regulated proteins that sense DNA damage and regulate the cell cycle machinery. For example, tumor suppressor p53 is activated to maintain genome stability, while CDC25 phosphatase is inhibited to prevent further cell cycle progression in response to DNA damage. The 14-3-3 family of phosphoserine/phosphothreonine binding proteins are involved in the regulation of DNA damage check point response, and they coordinate with DNA damage response regulators such as p53 and CDC25 to regulate the cell cycle to promote DNA repair or survival. Here, we discuss recent data that define the roles of 14-3-3 in DNA-damage checkpoint pathway.
Journal ArticleDOI
15 Mar 2022
TL;DR: The CDK2 (CDK2) as discussed by the authors is a cycle dependent kinas 2 (CBK2)-based CDK that uses a cyclin dependent kinase (CK) to detect cyclin cycles.
Abstract: Бүх амьд организмын амьдран тогтнох үндэс эсийн хуваагдал, түүний нарийн зохицуулга байдаг. Эсийн хуваагдлын бүхий л хугацааны туршид циклин-CDK хос уургууд бусад уургуудын хооронд харилцан үйлчлэлд орж, уургуудийн концентрацийн өөрчлөлтөөр эсийн хуваагдах үйл явц өрнөдөг. Зохицуулга алдагдвал хорт хавдар, удамшлын өвчин үүсэх шалтгаан болдог байна. Эсийн хуваагдлын зохицуулгын туршлагын болон онолын судалгаанууд эрчимтэй хийгдэж байна. Бид эсийн хуваагдлын G,->S шилжилтэнд оролцох уургуудын харилцан үйлчлэлд санамсаргүй хүчин зүйлийн нөлөөллийг тооцох симуляци хийлээ. Шилжилтэнд СусЕ (СусЕ, Cyclin Е'), CDK2 (CDK2, Cyclin dependent kinas 2), CDC25 уургууд оролцох бөгөөд эдгээр уургуудийн хооронд явагдах нийт 14 урвалын магадлалыг бичив. Урвалуудаас хэдий хугацаанд, аль урвал явахыг Монте Карло аргаар санамсаргүй тоонуудаар сонгож олно. Уураг тус бүрийн концентрацийг Ω параметрийн тусламжтайгаар молекулын тоо ширхэгт хөрвүүлж, төлөвийн өөрчлөлтийн вектороор молекулуудын тооны өөрчлөлтийг олно. Энэ алгоритмаар Matlab, Fortran програмууд дээр код бичиж бодлоо. Энэхүү бодолтонд молекулуудын тооны өөрчлөлт нь Ω параметрийн бага утганд үед санамсаргүй хүчин зүйлийн нөлөө их, харин их утганд ялангуяа Ω=200 үед санамсаргүй хүчин зүйлийн нөлөө бага бөгөөд динамик загварын шийдтэй төстэй болж байлаа. СусЕ уураг задрах, CDC25 уураг задрах, хоёр фосфортой CDC25 уураг задрах урвалын явагдах магадлал бага байсан учраас хасаж бодуулав. Эндээс харвал урвалын магадлал хэдий бага боловч эдгээр урвал эсийн хуваагдалд чухал нөлөөтэй болох нь харагдаж байна.
Journal ArticleDOI
TL;DR: Based on the amino acidsequences of the catalytic domains, over 100 protein tyro-sine phosphatases can be classified into four separate families: class I cysteine-based PTPs containing classicalPTPs and dual-specificity protein phosphatase (DSPs), and class II cysteinespecific low mole-cular weightosphatases.
Abstract: Based on the amino acidsequences of the catalytic domains, over 100 protein tyro-sine phosphatases can be classified into four separatefamilies: (i) class I cysteine-based PTPs containing classicalPTPs and dual-specificity protein phosphatases (DSPs), (ii)class II cysteine-based PTPs: tyrosine-specific low mole-cular weight phosphatases, (iii) class III cysteine-based PTPscontaining CDC25 homology (CH2) domain, and (iv) Eyesabsent (EyA) proteins as members of aspartic acid-basedPTPs.

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