Yali Dou

Dr. Yali Dou is a Professor in the Department of Medicine and Department of Biochemistry and Molecular Medicine. She is Marion and Harry Keiper Endowed Professor for cancer research. Dr. Dou is the Associate Director for Basic Science at Norris Comprehensive Cancer Center.

Dr. Dou has received a number of prestigious awards including the Leukemia & Lymphoma Society Scholar Award (2012), Stand Up to Cancer IRG Award (2011), AACR Gertrude B. Elion Cancer Research Award (2010) and Dean’s Award in Basic Science at University of Michigan (2014).

Research Interests
Cell fate decisions are controlled by transcription factors acting in concert with epigenetic regulators, which include enzymes that carry out histone post-translational modifications. Epigenetic mechanism underlies cell fate commitment and plasticity; its dysregulation emerges as a key characteristic of human malignancies. The Dou lab uses multidisciplinary approaches to study the establishment and maintenance of gene regulatory networks, focusing on how chromatin modifications exert temporal and spatial gene regulation via transcription factors and DNA regulatory elements. The lab is also interested in the interplays between chromatin modifications and other important cellular processes, including metabolic regulation, genome stability and higher order chromatin organization. In particular, Dou lab has extensive research on the MLL/KMT2 family of histone methyltransferases. MLL/KMT2 deposit histone H3 lysine 4 methylation, which prominently marks active gene promoters and distal enhancers. The MLL/KMT2 enzymes are frequently deleted, mutated or translocated in acute leukemia, solid tumors as well as a wide spectrum of human developmental syndromes. The study will not only advance understanding of the fundamental roles of epigenetic modulators in development and diseases, but also provide critical insights into designing novel target-based therapeutic strategies for cancer treatment and regenerative medicine.

• Author Correction: Quiescence enables unrestricted cell fate in naive embryonic stem cells Nat Commun. 2024 Mar 12; 15(1):2215. . View in PubMed
• Quiescence enables unrestricted cell fate in naive embryonic stem cells Nat Commun. 2024 Feb 26; 15(1):1721. . View in PubMed
• Non-canonical MLL1 activity regulates centromeric phase separation and genome stability Nat Cell Biol. 2023 Nov; 25(11):1637-1649. . View in PubMed
• Modeling kidney development, disease, and plasticity with clonal expandable nephron progenitor cells and nephron organoids bioRxiv. 2023 May 25. . View in PubMed
• Dissecting MENIN in bivalent gene regulation Nat Cell Biol. 2023 02; 25(2):209-210. . View in PubMed
• Structural insights on the KMT2-NCP interaction Biochem Soc Trans. 2023 02 27; 51(1):427-434. . View in PubMed
• Dysregulation of intercellular signaling by MOF deletion leads to liver injury J Biol Chem. 2021 Jan-Jun; 296:100235. . View in PubMed
• Histone Acetyltransferase MOF Blocks Acquisition of Quiescence in Ground-State ESCs through Activating Fatty Acid OxidationCell Stem Cell. 2020 09 03; 27(3):441-458. e10. . View in PubMed
• Cryo-EM structure of the human MLL1 core complex bound to the nucleosome Nat Commun. 2019 12 05; 10(1):5540. . View in PubMed
• HOXA9 Reprograms the Enhancer Landscape to Promote LeukemogenesisCancer Cell. 2018 10 08; 34(4):643-658. e5. . View in PubMed
• MLL1 Inhibition Reprograms Epiblast Stem Cells to Naive Pluripotency Cell Stem Cell. 2016 Apr 07; 18(4):481-94. . View in PubMed
• Hijacked in cancer: the KMT2 (MLL) family of methyltransferases Nat Rev Cancer. 2015 Jun; 15(6):334-46. . View in PubMed
• Targeting MLL1 H3K4 methyltransferase activity in mixed-lineage leukemia Mol Cell. 2014 Jan 23; 53(2):247-61. . View in PubMed
• The histone acetyltransferase MOF is a key regulator of the embryonic stem cell core transcriptional network Cell Stem Cell. 2012 Aug 03; 11(2):163-78. . View in PubMed

• An, Woojin
• Rice, Judd
• Farnham, Peggy
• Sha, Liang
• Ying, Qilong