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TFIID and MYB Share a Therapeutic Handshake in AML
Charles C. Bell, Mark A. Dawson Cancer Cell Volume 33, Issue 1, Pages 1-3 (January 2018) DOI: /j.ccell Copyright © 2017 Elsevier Inc. Terms and Conditions
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Figure 1 Targeting the MYB-TIIFD Interaction to Specifically Disrupt MYB-Dependent Oncogenic Transcription (A) Schematic representation of how MYB recruits TIIFD to potentiate a malignant gene expression program in AML. (B) Depletion of TAF12 facilitates the proteasomal degradation of MYB and results in impaired TFIID recruitment to MYB target genes. (C) Squelching of TAF12 with a non-functional TAF4 peptide can block the association between MYB-TAF12 and the rest of the TIIFD complex and phenocopy the effects of TAF12 depletion. Cancer Cell , 1-3DOI: ( /j.ccell ) Copyright © 2017 Elsevier Inc. Terms and Conditions
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