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Farnham, Peggy J. Department of Biochemistry and Molecular Biology, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, California.
- KAP1 and transcriptional silencing
- KAP1 and repair of damaged DNA
- KAP1 and apoptosis
- Should KAP1 be targeted for inhibition in tumors?
- Related Primary Literature
The protein KAP1 (also called TRIM28) is expressed at low to moderate levels in most normal tissues. However, it is upregulated (that is, it has increased expression) in many human cancers, and it has been suggested that inhibition of KAP1 function may be a rational approach for cancer treatment. KAP1 is involved in regulating several cellular pathways, and it is critical to define the normal role of KAP1 to understand how targeting KAP1 might affect tumor growth and/or response to chemotherapeutic agents. Studies in which the levels of KAP1 have been artificially manipulated have suggested that KAP1 plays different roles in different cells. For example, KAP1 has been shown to be essential both for maintaining the pluripotency (that is, the capacity to generate any cell type in the body) of embryonic stem cells and for allowing these stem cells to properly differentiate. Similarly, studies of adult cells have indicated that KAP1 can either promote or inhibit cell differentiation, depending on the cell type. Insight into how KAP1 can have such diverse functions has come from identifying its protein interaction partners. This article focuses on three KAP1-containing complexes that are proposed to inhibit transcription [the process by which deoxyribonucleic acid (DNA) is transcribed into ribonucleic acid (RNA), which is then translated into the proteins that function to create the different types of body cells], facilitate DNA repair (the process by which the cell identifies and corrects damaged regions of the genome), and inhibit apoptosis (a programmed cell death pathway that controls various aspects of normal development and helps rid the body of unwanted or damaged cells).
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