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- W4313356237 abstract "Abstract Naïve B cells proliferate differentially in response to various mitogenic signals. However, regardless of the initiating stimulus, B cells that progressed through one mitotic division gain the ability to divide up to 3–4 times in the absence of renewed stimulation. In contrast, cells that had not progressed through mitosis did not divide except when re-stimulated. These observations go against accepted dogma about cell cycle regulation, which posits that cells need to be re-stimulated after each division to progress through G1. To identify the basis for signal-independent cell division we compared cells that had undergone one division and those that had not by several assays. Our findings indicate that divided cells are already pre-programed to cross restriction (R) point. The characteristics of cells that have divided once include bigger cell size in G1, low levels of p27, hyper-phosphorylated Rb, high c-Myc and phospho-CDK2. High throughput CyTOF analysis at single cell level with 25 parameters suggested that the G1 state of once-divided cells differs significantly from the G1 phase of cells progressing through the first cell division cycle. RNA-seq analysis identified Birc5 (Survivin) which is an E2F target gene as highly expressed in the cells that have underwent signal-independent proliferation. Survivin as exclusively present in G1 phase of divided B cells and blocking it with its inhibitor (LLP3) halted the G1-S progression and therefore blocked signal independent proliferation. This in vitro model may recapitulate aspects of signal independent cell division seen in the dark zone of the germinal center (GC) and resolve mechanisms involved in various GC specific B cell lymphomas." @default.
- W4313356237 created "2023-01-06" @default.
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- W4313356237 date "2017-05-01" @default.
- W4313356237 modified "2023-10-16" @default.
- W4313356237 title "Commitment of mitosis in B cells: “before and after”" @default.
- W4313356237 doi "https://doi.org/10.4049/jimmunol.198.supp.136.9" @default.
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