Molecular and Cellular Biology, November 2009, p. 5639-5644, Vol. 29, No. 21
0270-7306/09/$08.00+0 doi:10.1128/MCB.00661-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
| MINIREVIEW |

Atherosclerosis Research Center, Key Laboratory of Human Functional Genomics,1 Department of Pathophysiology,2 Experimental Center for Basic Medical Sciences, Nanjing Medical University, Nanjing, Jiangsu 210029, China,3 Department of Biochemistry, Boston University School of Medicine, Boston, Massachusetts 021184
First identified as the master regulator of major histocompatibility complex II transcription, class II transactivator (CIITA) has since been implicated in a host of pathologies by modulating the transcription of multiple different genes. How CIITA caters to cell- and tissue-specific transcriptional needs is hotly debated and investigated. One of the possible mechanisms underlying spatiotemporal control of CIITA transcriptional activity is the posttranslational modification (PTM) machinery that refines certain amino acid residues of CIITA and hence alters its activity in response to specific cellular and environmental cues. This review discusses our current understanding of the PTM map of CIITA, how these modifications fine-tune its activity, and how the study of this area may lead to potential therapeutic strategies.
Published ahead of print on 31 August 2009.
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