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CREB-binding protein(CBP)and its homologue p300 are transcriptional co-activators of various sequence-specifictranscription factors that are involved in a wide array of cellular activities,such as DNA repair,cell growth,differentia-tion and apoptosis.Several studies have suggested that CBP and p300 might be considered as tumour suppressors,withtheir prominent role being the cross-coupling of distinct gene expression patterns in response to various stimuli.Theyexert their actions mainly via acetylation of histones and other regulatory proteins(e.g.p53).A major paradox in CBP/p300 function is that they seem capable of contributing to various opposed cellular processes.Respiratory epitheliumtumorigenesis represents a complex process of multi-step accumulations of a gamut of genetic and epigenetic aberra-tions.Transcription modulation through the alternate formation of activating and repressive complexes is the ultimateconverging point of these derangements,and CBP/p300 represents key participants in this interplay.Thus,illuminationof their molecular actions and interactions could reveal new potential targets for pharmacological interventions in re-spiratory epithelium carcinogenesis.
CREB-binding protein (CBP) and its homologue p300 are transcriptional co-activators of various sequence-specific transcription factors that are involved in a wide array of cellular activities, such as DNA repair, cell growth, differentiation and apoptosis. suggested that CBP and p300 might be considered as tumor suppressors, withtheir prominent role being the cross-coupling of distinct gene expression patterns in response to various stimuli.Theyexert their actions mainly via acetylation of histones and other regulatory proteins (egp53) .A major Paradox in CBP / p300 function is that they seem capable of contributing to various opposed cellular processes. Respiratory epithelium tumorigenesis represents a complex process of multi-step accumulations of a gamut of genetic and epigenetic aberra-tions. Transcription modulation through the alternate formation of activating and repressive complexes is the ultimateconverging point of these derangements, and CBP / p300 represents the key part icipants in this interplay.Thus, illuminationof their molecular actions and interactions could reveal new potential targets for pharmacological interventions in re-spiratory epithelium carcinogenesis.