• The cdc25 gene product is a tyrosine phosphatase that acts as an initiator of M-phase in eukaryotic cell cycles by activating p34 cdc2 . (biologists.com)
  • The presence of replication stress activates the DNA damage response and downstream checkpoint proteins including ataxia telangiectasia and Rad3 related kinase (ATR), checkpoint kinase 1 (CHK1), and WEE1-like protein kinase (WEE1), which trigger cell cycle arrest while protecting and restoring stalled replication forks. (bmj.com)
  • Inhibitory phosphorylation of MPF correlated with phosphorylation changes of cdc25C, the MPF phosphatase, and physical interaction of cdk1 with wee1, the MPF kinase, during M-phase exit. (ox.ac.uk)
  • Upon cloning these genes, Nurse and coworkers discovered that Cdc2 is definitely a serine/threonine proteins kinase and Wee1 is definitely a tyrosine/threonine proteins kinase. (healthandwellnesssource.org)
  • Small molecule inhibitors designed to target the DNA damage sensors, such as inhibitors of ataxia telangiectasia-mutated (ATM), ATR, CHK1 and WEE1, impair smooth cell cycle modulation and disrupt efficient DNA repair, or a combination of the above, have demonstrated interesting monotherapy and combinatorial activity, including the potential to reverse drug resistance and have entered developmental pipelines. (bmj.com)
  • Exogenous RRM2 expression rescued hallmarks of replication stress induced by co-inhibiting IGF with CHK1 or WEE1, identifying RRM2 as a critical target of the functional IGF:CHK1 and IGF:WEE1 interactions. (nature.com)
  • With characteristic extreme caution, Nurse [3] diagrammed the hereditary evidence as with Fig.?1b, although he speculated that Wee1 inhibited Cdc2 by phosphorylating it on neighboring threonine and tyrosine residues, and Cdc25 activated Cdc2 by promoting removing these phosphate organizations. (healthandwellnesssource.org)
  • Similar phenotypes were induced by IGF:WEE1 co-inhibition, also via exacerbation of RRM2 downregulation. (nature.com)
  • Wee1, conserved among all eukaryotes phosphorylates Tyr15, whereas members of the Cdc25 family are phosphatases, counteracting this activity. (wikipedia.org)
  • These results indicate that Nim1 regulates the mitotic process by rendering Wee1, a mititic inhibitor inactive. (readabstracts.com)
  • We characterize book Cks binding sites in the mitotic regulator Wee1 and find out a novel function for Cks in regulating Cdk activity at mitotic entrance. (conferencedequebec.org)
  • Dephosphorylation of Cdc2 by Cdc25 phosphatase(s) at positions T14 and Y15 leads to generation of active MPF heterodimers ( right ). (comprehensivephysiology.com)
  • 1997). Hyperphosphorylation of the N-terminal domain of Cdc25 regulates activity toward cyclin B1/cdc2 but not cyclin A/cdk2. (sdbonline.org)
  • We develop a high-throughput single-cell assay system of CDK activity in vivo and show that inhibitory tyrosine phosphorylation of CDK encodes cell size information, with the phosphatase PP2A aiding to set a size threshold for division. (elifesciences.org)
  • a family of dual threonine/tyrosine phosphatases. (nih.gov)
  • Results showed that overproduction of Nim1 led to the hyperphosphorylation of Wee1. (readabstracts.com)
  • Using a novel in vivo phosphatase assay, we also show that PP2A bound to Rts1 , the budding yeast B56-regulatory subunit, regulates dephosphorylation of Cdk1 independently of a function regulating Swe1 , Mih1 , or Ptp1 , suggesting that PP2A(Rts1) either directly dephosphorylates Cdk1-Y19 or regulates an unidentified phosphatase. (yeastgenome.org)
  • The detailed model could be used to explain various * experiments relevant to G2DDC reported recently, including the * nuclear export of 1433 bound Cdc25, the down-regulation of cyclin * B1 expression by p53, the effect of Chk1 and p53 on Cdc25 levels, * and Wee1 degradation. (nih.gov)
  • Exogenous RRM2 expression rescued hallmarks of replication stress induced by co-inhibiting IGF with CHK1 or WEE1, identifying RRM2 as a critical target of the functional IGF:CHK1 and IGF:WEE1 interactions. (nature.com)
  • Here we show that the phosphatase Ptp1 also regulates Cdk1 dephosphorylation in vivo and can directly dephosphorylate Cdk1 in vitro. (yeastgenome.org)
  • Wee1, conserved among all eukaryotes phosphorylates Tyr15, whereas members of the Cdc25 family are phosphatases, counteracting this activity. (wikipedia.org)
  • Wee1 is controlled upstream by Cdr1, Cdr2, and Pom1. (wikipedia.org)
  • The complete original paper reference is cited below: * * A quantitative analysis of the kinetics of the G2 DNA damage * checkpoint system, Baltazar D. Aguda, 1999 Proceedings of the * National Academy of Sciences, 96, 11352-11357 PubMed ID: 10500180 * * Figure 1 * * [[Image file: aguda_1999_ba.png]] * * Schematic diagram of the G2DDC system showing the subsystems * involving Wee1, MPF, Cdc25, and signal transduction pathways. (nih.gov)