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Volume 9, Issue 2, Pages (February 2002)

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Presentation on theme: "Volume 9, Issue 2, Pages (February 2002)"— Presentation transcript:

1 Volume 9, Issue 2, Pages 213-224 (February 2002)
CtBP, an Unconventional Transcriptional Corepressor in Development and Oncogenesis  G Chinnadurai  Molecular Cell  Volume 9, Issue 2, Pages (February 2002) DOI: /S (02)

2 Figure 1 Domain Structure and Functional Map of hCtBP1
The regions of highest homology with 2-hydroxy acid dehydrogenases are shown in red. The putative catalytic His residue is indicated. The regions required for mediating transcriptional repression of hCtBP1 and binding to the PXDLS motif are based on Koipally and Georgopoulos (2000). The dCtBP sequences required for repression (indicated by the thicker line) and transcriptional activation in mammalian cells are based on Phippen et al. (2000). The coordinates indicate hCtBP1 sequences that correspond to dCtBP. The sequences required for homodimerization (CtBP2) are based on Sewalt et al. (1999). For detailed sequence alignments with various CtBPs and dehydrogenases, see Turner and Crossley, 2001. Molecular Cell 2002 9, DOI: ( /S (02) )

3 Figure 2 CtBP Corepressor Complex
CtBP associates with DNA binding transcription factors either directly or through other proteins such as CtIP, RIP140, or class II HDACs as well as MIRT. Molecular Cell 2002 9, DOI: ( /S (02) )

4 Figure 3 Modulation of E1A Activities by CtBP
Three different models that may explain the effect of CtBP on E1A-mediated oncogenic transformation are presented. See the text for further details. Molecular Cell 2002 9, DOI: ( /S (02) )

5 Figure 4 Modulation of Wnt Signaling during Oncogenesis by CtBP
The (A)9 repeat frequently mutated in gastrointestinal tumors with MSI is indicated. Potential acetylation of the Lys residues adjacent to the CtBP binding motifs or frame shift mutations (due to deletion of an A residue) within the A(9) repeat may abolish CtBP interaction and facilitate trans-activation by β-catenin and CBP in tumor cells. Molecular Cell 2002 9, DOI: ( /S (02) )


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