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CBP HAT

Abbreviations CBP, CREB binding protein CREB, cAMP response element binding protein FAT, factor acetyltransferase HAT, histone acetyltransferase MEL, mixed lineage leukaemia protein MORE, MOZ related factor MOZ, monocytic leukaemia zinc finger protein PHD, plant homeodomain RTS, Rubinstein-Taybi syndrome, TIE, transcription intermediary factor... [Pg.233]

Figure 4. Leukaemic gene fusions involving HATs. (a) The t(8 16) translocation result in the MOZ-CBP fusion protein, while inv(8) gives rise to MOZ-T1F2. (b) Hypothetical model to explain how MOZ-T1F2 and MOZ-CBP fusions result in a similar leukaemia cell phenotype. See text for details, (c) The t(ll 16) and t(l 1 22) result in the MLL-CBP and MLL-p300 gene fusions, respectively... Figure 4. Leukaemic gene fusions involving HATs. (a) The t(8 16) translocation result in the MOZ-CBP fusion protein, while inv(8) gives rise to MOZ-T1F2. (b) Hypothetical model to explain how MOZ-T1F2 and MOZ-CBP fusions result in a similar leukaemia cell phenotype. See text for details, (c) The t(ll 16) and t(l 1 22) result in the MLL-CBP and MLL-p300 gene fusions, respectively...
Figure I. Chromatin acetylation status, transcription and survival a balance between HAT and HDAC activities, (a) Transcriptional activationlrepression relies on the chromatin acetylation status of histones. TBP TATA-Binding Protein, TF Transcription Factor, TR Transcriptional Repressor, (b) A fine-tuning of HAT/HDAC activities orchestrates neuronal death and survival. On one hand, acetylation levels can be decreased (HypoAc) because of CBP loss of function, as observed during apoptosis and neurodegeneration. On the other hand, when the threshold of acetylation is exceeded (HyperAc), this ultimately leads to nemonal death. (See Colom Plate 16.)... Figure I. Chromatin acetylation status, transcription and survival a balance between HAT and HDAC activities, (a) Transcriptional activationlrepression relies on the chromatin acetylation status of histones. TBP TATA-Binding Protein, TF Transcription Factor, TR Transcriptional Repressor, (b) A fine-tuning of HAT/HDAC activities orchestrates neuronal death and survival. On one hand, acetylation levels can be decreased (HypoAc) because of CBP loss of function, as observed during apoptosis and neurodegeneration. On the other hand, when the threshold of acetylation is exceeded (HyperAc), this ultimately leads to nemonal death. (See Colom Plate 16.)...
An explanation for this net deacetylation throughout neurodegeneration is that neuronal cells progressively lose a HAT, and more particularly, the CREB binding protein (CBP) (reviewed below and in (Rouaux et al, 2004 Saha and Pahan 2006)... [Pg.274]


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See also in sourсe #XX -- [ Pg.191 ]




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