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The G2 M mitotic transition is regulated by cyclin-dependent kinase 1 (CDK1) that associates with the regulator cyclin-B1.
G2/M transition is regulated by the cyclin B1/CDC2 complex [ 15], and MDM2 is a negative regulator of p21, which is involved in the G2/M checkpoint and is required for cell cycle arrest in the G2/M2 phase [ 16, 17].
Thus, MCM, Cdc45, and PCNA loading in late-G1 or at the G1-S transition is regulated at the post-transcriptional level in CHO cells, consistent with our findings in MK cells.
We demonstrated that this transition is regulated by FSH/cAMP/MAPK-sox9 pathway.
Ubiquitination of p27 at the G1/S transition is regulated by its phosphorylation [ 116].
The G2/M transition is regulated by the sequential activation and inactivation of the cdc2/cyclin B complex [ 19].
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In Drosophila and other insects these developmental transitions are regulated by the coordinate action of two principal hormones, the steroid ecdysone and the sesquiterpenoid juvenile hormone (JH).
Dormancy transitions are regulated by short photoperiods and/or chilling temperatures.
The PTP open-closed transitions are regulated by physiological effectors, and the consequences of pore opening vary dramatically depending on the open time [16].
The reversible solution-hydrogel transitions are regulated by changing the balance between hydrophobic interactions and electrostatic repulsion of the silk nanofibers.
Physiological and genetic studies have demonstrated that both developmental transitions are regulated not only by environmental signals such as day length, light intensity, and ambient temperature, but also by endogenous signals transmitted by plant hormones and age.
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