|Description||Guava Cell Cycle Reagent for Flow Cytometry|
|Overview||For researchers who want to do cell cycle research at their benchtop, the Guava® Cell Cycle Assay can be used for measuring G0/G1, S, and G2/M phase distributions.
Easy and convenient
Based on the established method of whole-cell staining with propidium iodide (PI), the Guava Cell Cycle Assay is easy to learn. Guava Cell Cycle Software includes markers that can be set for quick assessment of G0/G1, S, and G2/M phase cell cycle percentages as data is being collected for rapid screening of compounds. Results are automatically exported to a spreadsheet; raw data can also be exported to third-party software for cell cycle analysis using modeling algorithms.
Whether you are a researcher exploring the mitotic pathway, or evaluating novel compounds for cancer therapies, you will appreciate the ease and convenience of doing cell cycle studies, right in your lab. For use with all instruments. Click here for more information regarding Instrument Compatibility
|Application||For researchers who want to do cell cycle research at their benchtop, the Guava Flow Cytometer Cell Cycle Assay can be used for measuring G0/G1, S & G2/M phase distributions.|
|Safety Information according to GHS|
|Storage and Shipping Information|
|Material Size||100 Tests|
|Guava® Cell Cycle Reagent - 12-0213||12-0213|
|Guava® Cell Cycle Reagent - 12-0521||12-0521|
|Guava® Cell Cycle Reagent - 12-0578||12-0578|
|Guava® Cell Cycle Reagent - 13-0477||13-0477|
|Reference overview||Pub Med ID|
|Dysfunction of nucleus accumbens-1 activates cellular senescence and inhibits tumor cell proliferation and oncogenesis.|
Zhang, Yi, et al.
Cancer Res., 72: 4262-75 (2012) 2012
Nucleus accumbens-1 (NAC1), a nuclear factor belonging to the BTB/POZ gene family, has emerging roles in cancer. We report here that NAC1 acts as a negative regulator of cellular senescence in transformed and nontransformed cells, and dysfunction of NAC1 induces senescence and inhibits its oncogenic potential. We show that NAC1 deficiency markedly activates senescence and inhibits proliferation in tumor cells treated with sublethal doses of γ-irradiation. In mouse embryonic fibroblasts from NAC1 knockout mice, following infection with a Ras virus, NAC1(-/-) cells undergo significantly more senescence and are either nontransformed or less transformed in vitro and less tumorigenic in vivo when compared with NAC1(+/+) cells. Furthermore, we show that the NAC1-caused senescence blunting is mediated by ΔNp63, which exerts its effect on senescence through p21, and that NAC1 activates transcription of ΔNp63 under stressful conditions. Our results not only reveal a previously unrecognized function of NAC1, the molecular pathway involved and its impact on pathogenesis of tumor initiation and development, but also identify a novel senescence regulator that may be exploited as a potential target for cancer prevention and treatment. Cancer Res; 72(16); 4262-75. ©2012 AACR.
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