2pp4
Solution Structure of ETO-TAFH refined in explicit solvent
Structural highlights
DiseaseMTG8_HUMAN Note=A chromosomal aberration involving RUNX1T1 is a cause of acute myeloid leukemia (AML-M2). Translocation t(8;21)(q22;q22) with RUNX1/AML1.[1] [2] [3] [4] Defects in RUNX1T1 may be a cause of colorectal cancer (CRC) [MIM:114500. FunctionMTG8_HUMAN Transcription regulator that excerts its function by binding to histone deacetylases and transcription factors. Can repress transactivation mediated by TCF12.[5] [6] Evolutionary Conservation Check, as determined by ConSurfDB. You may read the explanation of the method and the full data available from ConSurf. Publication Abstract from PubMedThe eight twenty-one protein, ETO, is implicated in 12%-15% of acute human leukemias as part of a gene fusion with RUNX1 (also called AML1). Of the four ETO domains related to Drosophila melanogaster Nervy, only two are required to induce spontaneous myeloid leukemia upon transplantation into the mouse. One of these domains is related in sequence to TAF4, a component of TFIID. The structure of this domain, ETO-TAFH, is similar to yeast Rpb4 and to Escherichia coli sigma(70); it is the first TAF-related protein with structural similarity to the multisubunit RNA polymerases. Overlapping surfaces of ETO-TAFH interact with an autonomous repression domain of the nuclear receptor corepressor N-CoR and with a conserved activation domain from the E-box family of transcription factors. Thus, ETO-TAFH acts as a structural platform that can interchange negative and positive coregulatory proteins to control transcription. A TAF4-homology domain from the corepressor ETO is a docking platform for positive and negative regulators of transcription.,Wei Y, Liu S, Lausen J, Woodrell C, Cho S, Biris N, Kobayashi N, Wei Y, Yokoyama S, Werner MH Nat Struct Mol Biol. 2007 Jul;14(7):653-61. Epub 2007 Jun 17. PMID:17572682[7] From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. References
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