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Douglas Barrows on Muck Rack

Douglas Barrows

As seen in: Nature, PNAS, BioRxiv, Cell Press, Cell Stem Cell, Texas Medical Center, The Journal of Biological Chemistry
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Articles

Molecular mechanisms of the MLL4 complex in H3K4 methylation and p53-dependent transcription activation

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By Jianfeng Sun, Zhiying Zhang, You Yu, Nicole Cruz, Sicong Zhang, Yufei Xiang, Keiichi Ito, Cole Lazarus, Zhanyun Tang, Buren Li, Douglas Barrows, Tom W. Muir, Yi Shi, Dina Schneidman-Duhovny, Shu-Ping Wang, Linas Urnavicius, Dinshaw J. Patel, Robert G. Roeder
| Cell Press Verified
Keywords MLL4 p53 H3K4 methylation transcriptional regulation nucleosome binding coactivator synergy epigenetic crosstalk Introduction Histone H3K4 methylation is a highly conserved post-translational modification intricately linked to transcription activation in eukaryotic cells.
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The conserved N-terminal SANT1-binding domain (SBD) of EZH2 Regulates PRC2 Activity

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By Yadira M Soto-Feliciano, Douglas Barrows, Laiba Khan, Agata Lemiesz Patriotis
| BioRxiv
Abstract Polycomb group proteins maintain gene expression patterns established during early development, with Polycomb Repressive Complex 2 (PRC2) methyltransferase a key regulator of cell differentiation, identity and plasticity. Consequently, extensive somatic mutations in PRC2, including gain- or loss- of function (GOF or LOF), are observed in human cancers.
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"A Molecular Switch between Mammalian MLL Complexes Dictates Response t" by Yadira M Soto-Feliciano, Francisco J Sánchez-Rivera et al.

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By Yadira M Soto-Feliciano, Francisco J. Sanchez-Rivera, Florian Perner, Douglas Barrows
| Texas Medical Center
Abstract Menin interacts with oncogenic MLL1-fusion proteins, and small molecules that disrupt these associations are in clinical trials for leukemia treatment. By integrating chromatin-focused and genome-wide CRISPR screens with genetic, pharmacologic, and biochemical approaches, we discovered a conserved molecular switch between the MLL1-Menin and MLL3/4-UTX chromatin-modifying complexes that dictates response to Menin-MLL inhibitors.
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