Gene interactions and pathways from curated databases and text-mining

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CDC26 — PCNA

Text-mined interactions from Literome

Zachariae et al., Curr Opin Cell Biol 1999 : Progression through mitosis is controlled by cyclin dependent kinases, which drive cells into metaphase, and by the anaphase promoting complex/cyclosome , a ubiquitin ligase that triggers sister chromatid separation and exit from mitosis
Tyson et al., J Theor Biol 2001 : First, we present a simple model of the antagonistic interactions between cyclin dependent kinases and the anaphase promoting complex , which shows how progress through the cell cycle can be thought of as irreversible transitions ( Start and Finish ) between two stable states ( G1 and S-G2-M ) of the regulatory system
Gopalakrishnan et al., Proc Natl Acad Sci U S A 2001 : Cdc18 is negatively controlled by cyclin dependent kinase (CDK) phosphorylation, but low level expression of a mutant form of Cdc18 lacking CDK phosphorylation sites ( Cdc18 ( CDK ) ) is not sufficient to induce rereplication
Irniger et al., FEBS Lett 2002 : Cyclin proteolysis is triggered by the anaphase promoting complex/cyclosome ( APC/C ), a multi-subunit complex which contains ubiquitin ligase activity
Guardavaccaro et al., Dev Cell 2003 (Infertility, Male) : Furthermore, cyclin A, cyclin B, and Emi1, an inhibitor of the anaphase promoting complex , are stabilized in mitotic beta-Trcp1 ( -/- ) MEFs
Margottin-Goguet et al., Dev Cell 2003 : Progression through mitosis occurs because cyclin B/Cdc2 activation induces the anaphase promoting complex (APC) to cause cyclin B destruction and mitotic exit
Archambault et al., Expert Rev Proteomics 2005 : In the past 5 years, developments in mass spectrometry based proteomics have been applied to the study of protein interactions and post-translational modifications involving key cell cycle regulators such as cyclin dependent kinases and the anaphase promoting complex , as well as effectors such as centrosomes, the kinetochore and DNA replication forks
Gu et al., Mol Cancer Ther 2006 (Skin Neoplasms) : Silibinin caused decrease in E2F2 and E2F3 was accompanied by reduced levels of cyclin dependent kinases, cyclins, CDC25C , and mitogen activated protein kinases and Akt signaling and inhibition of cell proliferation
Ban et al., Dev Cell 2007 : Cyclin dependent kinase 1 (Cdk1) initiates mitosis and later activates the anaphase promoting complex/cyclosome ( APC/C ) to destroy cyclins
Kang et al., Hum Pathol 2009 (Breast Neoplasms...) : Cyclin B proteolysis is triggered by the anaphase promoting complex
Singh et al., Clin Cancer Res 2009 (Prostatic Neoplasms) : Decreased levels of cyclin dependent kinases 2, 4, and 6, CDC2 , and cyclins D1, D3, E, and A were observed, indicating an inhibitory effect of silibinin on cell cycle progression
Wijnker et al., Plant reproduction 2013 : Progression through meiosis relies on many of the same, or at least homologous, cell cycle regulators that act in mitosis, e.g., cyclin dependent kinases and the anaphase promoting complex/cyclosome
Gerber et al., Proc Natl Acad Sci U S A 1995 : We have investigated the role of Cdc37 in the regulation of the cyclin dependent protein kinase Cdc28
Elsasser et al., Mol Biol Cell 1996 : During purification of recombinant Cdc6 expressed in yeast, we found that Cdc6 interacts with the critical cell cycle, cyclin dependent protein kinase Cdc28. Cdc6 and Cdc28 can be coimmunoprecipitated from extracts, Cdc6 is retained on the Cdc28 binding matrix p13-agarose, and Cdc28 is retained on an affinity column charged with bacterially produced Cdc6
Amon et al., EMBO J 1997 : Cln-Cdc28 kinase activity at START is required to repress B-type cyclin-specific proteolysis
Charles et al., Curr Biol 1998 : We investigated the role of Cdc5 in the regulation of mitotic cyclin degradation
Cross et al., Mol Cell Biol 1998 : The enzymatic and biological activity of the mutant Cdc28p was essentially normally regulated by cyclin , and the mutants supported normal cell cycle progression and regulation
Edgington et al., Mol Cell Biol 1999 : A specific amino acid substitution in the cyclin dependent protein kinase Cdc28 was found to cause constitutive expression of most filamentous growth characteristics