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These cleavage cycles represent the minimal cell cycle, alternating between genome replication (S-phase) and genome segregation (M-phase) and lacking gap phases (G1 and G2-phase) and cell cycle checkpoints.
This compound is an inducer of protein kinase C activity which stimulates HIV-1 expression in latently-infected lymphoid and myeloid cell lines and primary cells [22], [23], [24], [25], [26], [27], [28], [29] with minimal effects on the immune system [26] and causing minimal cell cycle progression [26], [29].
If the regulation of Cdc2 activity is necessary and sufficient for a minimal cell cycle, this implies that other cyclin CDK combinations may have additional roles [ 16].
This minimal cell cycle is responsible for the rapid and synchronous division seen in early-stage invertebrate and anamniote embryos and is driven by alternating CDK2 (S-phase) and Cdc2 (M-phase) activities.
Indeed the expression of the Notch downstream target, Hes1, is known to oscillate at rates much shorter than the minimal cell cycle time in neural progenitor cells in culture, and pairs of interacting cells may oscillate out of phase with each other [ 50].
In mt- p53 cells, prominent GUT-70-induced apoptosis was accompanied by minimal cell cycle arrest, which is consistent with a previous report of G2/M checkpoint abrogation in p53/p21-impaired p53/p21-impairedwnregulation of cellsand Wee1 by Hsp90 inhibithrought resultedownregulation mitofiChk1try and mitotic death (Tse et al, 2009).
Similar(54)
In vitro, grl knockdown (KD) in differentiated venous endothelial cells (ECs) resulted in minimal changes in cell cycle.
Using this line, we found that the drug had minimal effect on cell cycle profiles, cellular proliferation, or the expression of other cellular or latent viral proteins, indicating that the RTA suppression was not a result of global cellular dysregulation.
As shown in Table 6, AZD7762 alone exhibited a minimal effect on cell cycle distribution, TH-302 alone induced concentration-dependent cell cycle arrest at G2/M, and at higher concentrations, TH-302 also induced a profound S phase arrest.
However, only minimal changes in cell cycle and proliferation (data not shown) were observed following specific ablation of EpCAM expression in MDA-231 breast cancer cells under these experimental conditions.
Depletion of BRCA1 reduced 4OHT-induced HR in U2OS HR NEIE cells, in comparison to control siRNA, but with minimal disruption of the cell cycle profile (Figure 4B).
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