Imed Gallouzi
Professor Emeritus, Department of Biochemistry
1998 - PhD, Graduate School of Biology and Health, Montpellier, France
mÏ㽶ÊÓƵ metabolism during the cell cycle; cell differentiation
Our general research area is mÏ㽶ÊÓƵ metabolism during the cell cycle and cell differentiation. We use the tools of molecular and cell biology to study problems in this field. The long-term research goals focus on understanding the cellular mechanisms involved in the regulation of mÏ㽶ÊÓƵ half-lives and how they affect cell growth and differentiation.
mÏ㽶ÊÓƵ stability influences gene expression in virtually all organisms, from bacteria to mammals. In mammalian cells, the abundance of a particular mÏ㽶ÊÓƵ can fluctuate dramatically due to a change in mÏ㽶ÊÓƵ half-life, without any change in transcription. The processes that regulate mÏ㽶ÊÓƵ half-lives can thus affect how a cell grows, differentiates and responds to its environment.
Understanding these processes requires a combination of different approaches; molecular biology and biochemistry techniques will help to understand the molecular mechanisms by which mÏ㽶ÊÓƵ stability and degradation are regulated during cell division and differentiation and the cell biological technology will help to establish the connection between them. Towards these goals, we are using and developing in vitro, in vivo and ex-vivo methods to facilitate the identification and the characterization of factors involved in the stabilization as well as in the degradation of mÏ㽶ÊÓƵs in mammalian cells.
Although these two phenomena are well-studied separately, very little is known about how they are integrated inside the cell. We do not know the factors that bridge and thus allow cross talk between the two processes. Since many cancer cells exhibit changes in mÏ㽶ÊÓƵ half-lives, a precise balance between the two processes is needed to preserve cell integrity. Therefore, it is important to define the link between mÏ㽶ÊÓƵ stabilization and degradation, and to establish how both are regulated inside the cell. Making this connection will help to clarify how and why many cancers start and will provide new targets for future therapy.
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