Hormonal Control of Cell Cycle (Research and Perspectives in by Shlomo Melmed, Henri Rochefort, Philippe Chanson

By Shlomo Melmed, Henri Rochefort, Philippe Chanson

This publication covers issues that variety from primary experiences of DNA replication, chromosomal and nuclear functionality via development issue keep watch over of endocrine tumor initiation and development. the fundamental and translational insights won from Hormonal keep an eye on of phone Cycle should be of curiosity to these learning the biology of endocrine tumors in addition to these deriving novel healing ways for those benign and malignant problems.

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Extra resources for Hormonal Control of Cell Cycle (Research and Perspectives in Endocrine Interactions)

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There are two important determinants of the ability of these cells to respond to IGF-I with an increase in proliferation. The first is that the signaling protein, Shc, must be recruited to the cell membrane and phosphorylated. Induction of Shc phosphorylation results in enhancement of MAP kinase activity, which is required for an increase in cell division. In order for these cells to undergo a mitogenic response and for Shc to be phosphorylated, the signaling protein IRS-1 must be down regulated, which occurs in these cells in response to hyperglycemic stress.

Vascular smooth muscle cells (SMC) are a useful model for studying cell cycle regulation because they maintain a stable, partially dedifferentiated phenotype in vitro and their phenotypic characteristics are similar to the characteristics of vascular SMC that proliferate in whole animal models following vascular injury. Exposure of cultured SMC to serum results in a doubling within 48 hr. In contrast, these cells require the induction of cell stress to proliferate in response to IGF-I. Hyperglycemia serves as a model of cell stress in this test system.

Cyclin E was shown to be loaded onto chromatin in Xenopus extracts (Chevalier et al. 1996; Furstenthal et al. 2001), where it interacts with DNAbound CDC6 (Furstenthal et al. 2001). This loading of cyclin E did not require CDK kinase activity, as addition of the chemical CDK inhibitor, roscovitine, had no effect on cyclin E chromatin recruitment (Furstenthal et al. 2001). These observations raise the possibility that cyclin E might form a physical “bridge” between components of the pre-replication complexes and MCMs, thereby contributing to MCM loading.

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