G1 stage

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G1 stage

the first growth phase of the eukaryotic CELL CYCLE.
References in periodicals archive ?
In the present results, the percentages of U266 and RPMI 8226 cells at G1 phase were notably increased by SKPin C1.
How stem cells manage to quickly transition through the G1 phase without risking incomplete MCM loading and resultant DNA damage has been a mystery.
Senescence is the result of cellular stresses, including DNA damage, that give rise to a cell cycle arrest in the G1 phase of the cell cycle; it involves the accumulation of the cell cycle inhibitor p16INK4A.and a collection of other proteins, including SA-bGal, whereas differentiation does not.
The length of G1 phase has been shown to determine the cellular fate of NSCs or NPCs [28].
[43] showed that the cell proportion of the S phase (13.56%) was obviously reduced, whereas the cell proportion of the G1 phase (85.20%) was obviously greater compared with normal control cells with S phase fraction of 21.82% and G1 phase fraction of 61.94% after the WI-38 cells were treated with [H.sub.2][O.sub.2].
Two main limit points are found, that is, 1G/S limit points (from G1 phase to S phase control cells can prevent the damage of base replication and repair mutation of chromosome) and G2/M limit point (cells in two control points can make the cell before the split phase repairing on the duplicated DNA damage).
Results: AB23 obviously inhibited proliferation of the three ovarian cancer cell lines, down-regulated the protein levels of CDK4, CDK6, and cyclin Dl, and blocked the cell cycle progressions in G1 phase. Meanwhile, AB23 induced accumulation of the sub-G1 phase in the three cell lines in a concentration dependent manner.
At early G1 phase, the Cyclin/CDK complex hypo-phosphorylate pRB, which block cell cycle progression into S-phase by sequestering the E2F family of transcription factors.
The percentage of cells in the G1 phase increased in a dose-dependent manner [Figure 3]b].
The use of natural compounds that stop cancer in G1 phase of the cell cycle may provide an alternative to 5-FU drug regime.
5-FU and liquiritigenin could significantly inhibit hepatoma cell progression from G1 phase to S phase, where G0/G1 phase cells increased, S phase cells decreased, and G2/M phase cells relatively increased.
By comparing the experimental results of groups (a)-(c), it was not difficult to see that after 24 hours interaction between Tubeimoside 1 and HepG2 cells, the ratio of HepG2 cells in G1 phase decreased gradually while the HepG2 cells in G2-M phase and S phase increased gradually with the increase of the concentration of Tubeimoside 1.