Thus, loss of p53 accelerated tumor onset but not the overall tumor incidence after 9 mpf.
MPF degradation further weakens the MPF activation loop promoting MPF inhibitory phosphorylation.
First, some kind of "initiator"—a signal independent of MPF allows the production of a small amount of MPF (i.e., "primary MPF") from preMPF.
Images show the result of dynamics applied to these noisy patterns using networks with all-to-all MPF parameters after L-BFGS training on (50text000) 64-cliques (({approx}2mathrm{e}31%) of all 64-cliques), Large deviation parameters ((x, y, z) = (0.0091, 0, 1)), or MPF Theory parameters ((x, y, z) = (0.0107, 0, 1)) from Eq. (7) in the main text.
The transition is triggered by cyclin concentration exceeding a threshold for MPF activation; after the transition is made, the cell remains in a mitotic state as cyclin concentration drops in anaphase and telophase, until the reverse transition (mitosis-to-interphase) is triggered at the other turning point of the S-shaped curve.
These points account for the previously confusing behavior of MPF in starfish, explaining both why MPF detection in starfish oocytes is easier after NEBD than before NEBD, and why MPF is detectable in the nucleus but not in the cytoplasm before NEBD.
To rule out that our findings were influenced by seasonal or daytime effects, we tested whether those parameters for which we found context-specific modulation (lowest MPF, song density, and CV of MPF) changed with the time of the day (measured as minutes after sunrise) and the season (measured as number of days after the start of the experiment).
In oocytes without protrusions after OA.5h treatment, while the MPF activity did not change, MAPK activities increased significantly (Figure 2C).
Differences include several amino acid variations near the N-terminus (amino acids 4 56) and a small insert in variant 2 compared to variant 1 after amino acid 410 of MPF (NP_005814).
Results from the present study demonstrate that the inhibitory effects of G-1 on cell proliferation are not explained by a disruption of the molecular control of cell-cycle progression, considering that histone H3 and MPF activity was normal after G-1 treatment.
