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They validated these insights by analyzing cell cycle regulation in fission yeast.
We started a characterization of the observed growth inhibition by analyzing cell cycle distribution patterns after chemotherapy.
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By analyzing cell-cycle sorted primary mouse lymphocytes we found that the 3D telomere organization changes during the cell cycle.
To investigate the molecular mechanism involved in potentiation of radiation-induced cell killing by genistein, we analyzed cell cycle progression and expression of molecules known to affect cell cycle regulation.
We analyzed cell cycle by fluorescence-activated cell sorting (FACS).
We analyzed cell cycle distribution by flow cytometry DNA deconvolution at 4, 12 and 24 h after treatment.
We analyzed cell cycle progression by flow cytometry since cell proliferation, survival, and DNA replication were downregulated in the Akt2-ablated cells.
To determine if 13-1-e has affect on cell cycle we isolated primary cells from the control and treated zebrafish embryos and analyzed cell cycle progression by fluorescence activated cell sorting (FACS) analysis.
To further characterize glioma cell response to SAHA and VPA, we next analyzed cell cycle distribution by flow cytometry.
Cell growth inhibition was confirmed by analyzing the cell cycle profile for each cell line after 72 h of treatment.
Three ovarian cancer cell lines, HEY, SKOV3, and IGROV-1, were assayed for glutamine dependence by analyzing cytotoxicity, cell cycle progression, apoptosis, cell stress, and glucose/glutamine metabolism.
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