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      저자 : Souad Ahmad Engliez (검색결과 2 건)
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        6-Aminonicotinamide induces G1 arrest by elevating p27kip1 as well as inhibiting cdk2, cyclin E and p-Rb in IMR32 neuroblastoma cell line

        Souad Ahmad Engliez,In Kook Park 한국통합생물학회 2005 Animal cells and systems Vol.9 No.4

        The effects of 6-aminonicotinamide (6-AN) on viability of IMR32 neuroblastoma cells in the presence of ATP or NAD+ have been investigated. 6-AN caused marked reduction in cell viability and similar observations were also made with cells treated with 6-AN+ATP. However, cells treated with 6-AN+NAD+ showed cell viability similar to untreated cells. Morphologically, 6-AN and 6-AN+ATP treated cells showed loss of neurites, polyhedric shapes, shrinkage of cell bodies and formation of lysed cells, while 6-AN+NAD+ cells did not show any such changes. The flow cytometry analysis demonstrated that 6-AN increased cell population in G0/G1 phase and decreased cell population in S and G2/M phase following a 72 h exposure. Western blot analysis showed that 6-AN stimulated a substantial increase in the level of the cdk inhibitor p27kip1, but lowered the levels of cdk2, cyclin E and p-Rb. However, cdc25A and p53R2 were not significantly affected. Immunofluorscence staining of p27kip1, cdk2, cyclin E and p-Rb revealed close correlation between the signal observed in the Western blot analysis. 6-AN+ATP treated cells showed similar results obtained with 6-AN treated cells in expression of cdk2, cyclin E, p-Rb proteins and p27kip1. 6-AN+NAD+cells showed greater expression of cdk2, cyclin E and p-Rb than those in 6-AN and 6-AN+ATP treated cells. The results suggest that 6-AN induced the G0/G1 phase arrest in IMR32 neuroblastoma cell lines through the increase of p27kip1 and the decrease of cdk2, cyclin E and p-Rb.

      • 6-Aminonicotinamide Induces $G_1$ Arrest by Elevating $p27^{kip1}$ as well as Inhibiting cdk2, Cyclin E and p-Rb in IMR32 Neuroblastoma Cell Line

        Engliez Souad Ahmad,Park In-Kook The Korean Society for Integrative Biology 2005 Integrative biosciences Vol.9 No.4

        The effects of 6-aminonicotinamide (6-AN) on viability of IMR32 neuroblastoma cells in the presence of ATP or $NAD^+$ have been investigated. 6-AN caused marked reduction in cell viability and similar observations were also made with cells treated with 6-AN+ATP. However, cells treated with $6-AN+NAD^+$ showed cell viability similar to untreated cells. Morphologically, 6-AN and 6-AN+ATP treated cells showed loss of neurites, polyhedric shapes, shrinkage of cell bodies and formation of lysed cells, while $6-AN+NAD^+$ cells did not show any such changes. The flow cytometry analysis demonstrated that 6-AN increased cell population in $G_0/G_1$ phase and decreased cell population in Sand $G_2/M$ phase following a 72 h exposure. Western blot analysis showed that 6-AN stimulated a substantial increase in the level of the cdk inhibitor $p27^{kip1}$, but lowered the levels of cdk2, cyclin E and p-Rb. However, cdc25A and p53R2 were not significantly affected. Immunofluorscence staining of $p27^{kip1}$, cdk2, cyclin E and p-Rb revealed close correlation between the signal observed in the Western blot analysis. 6AN+ATP treated cells showed similar results obtained with 6-AN treated cells in expression of cdk2, cyclin E, p-Rb proteins and $p27^{kip1}$, $6-AN+NAD^+$ cells showed greater expression of cdk2, cyclin E and p-Rb than those in 6-AN and 6-AN+ATP treated cells. The results suggest that 6-AN induced the $G_0/G_1$ phase arrest in IMR32 neuroblastoma cell lines through the increase of $p27^{kip1}$ and the decrease of cdk2, cyclin E and p-Rb.

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