A photo of Hee Woong Lim.

Member, Division of Biomedical Informatics

Assistant Professor, UC Department of PediatricsUC Department of Biomedical Informatics

513-803-0333

Biography & Affiliation

Biography

I trained to be a computational scientist. However, after obtaining my PhD, I had a fascination with the convoluted and multifaceted, yet very ordered, biological system. Therefore, I moved my career in the direction of the bioinformatics field for my postdoctoral training at the University of Pennsylvania.

During my postdoc, I studied transcriptional regulations in multiple metabolic systems, including liver, adipose tissues and pancreas. Then, I joined the team in the Division of Biomedical Informatics at the Cincinnati Children’s Hospital Medical Center as an assistant professor and started a regulatory genomics laboratory to further my research.

In my research lab, I study fundamental mechanisms of gene transcriptional regulations in various contexts, such as metabolism, general cellular or tissue development, pathogenesis, and pharmacogenomics. In particular, I focus on enhancer regulations to delineate their intrinsic heterogeneity of architectures and functions using a high-resolution landscape of transcription factor binding and enhancer RNA (eRNA). To this end, my lab actively utilizes multi-omics high-throughput data including GRO-seq, RNA-seq, ChIP-seq, ChIP-exo, CUT&RUN, csRNA-seq, etc.

The most notable discoveries I made over the years include using eRNAs for direct monitoring of enhancer activities to uncover a molecular mechanism of anti-diabetic rosiglitazone-driven gene transcriptional regulation and an unconventional role of HDAC3 to prepare a thermogenic program in brown fat. In addition, I have discovered distinct binding modes (dimeric and monomeric binding) of the glucocorticoid receptor (GR) by studying the high-resolution footprints of GR binding using ChIP-exo.

I have more than 10 years of experience in the biomedical informatics field and began working at Cincinnati Children’s Hospital Medical Center in 2019. My research has been published in respected journals, such as Nature, Cell, Genome Research, Genes and Development, Proceedings of the National Academy of Sciences of USA, and Genome Research.

Research Interests

Regulatory genomics; enhancer; transcription; metabolism; pharmacogenomics; machine learning

Academic Affiliation

Assistant Professor, UC Department of PediatricsUC Department of Biomedical Informatics

Divisions

Biomedical Informatics

Education

BS: Seoul National University, Seoul, Korea.

MS: Seoul National University, Seoul, Korea.

PhD: Seoul National University, Seoul, Korea.

Postdoc: University of Pennsylvania, Philadelphia, PA.

Publications

Selected Publication

Distinct macrophage populations direct inflammatory versus physiological changes in adipose tissue. Hill, DA; Lim, HW; Kim, YH; Ho, WY; Foong, YH; Nelson, VL; Nguyen, HC B; Chegireddy, K; Kim, J; Habertheuer, A; et al. Proceedings of the National Academy of Sciences of USA. 2018; 115:E5096-E5105.

Histone deacetylase 3 prepares brown adipose tissue for acute thermogenic challenge. Emmett, MJ; Lim, H; Jager, J; Richter, HJ; Adlanmerini, M; Peed, LC; Briggs, ER; Steger, DJ; Ma, T; Sims, CA; et al. Nature. 2017; 546:544-548.

Genetic Variation Determines PPARγ Function and Anti-diabetic Drug Response in Vivo. Soccio, RE; Chen, ER; Rajapurkar, SR; Safabakhsh, P; Marinis, JM; Dispirito, JR; Emmett, MJ; Briggs, ER; Fang, B; Everett, LJ; et al. Cell. 2015; 162:33-44.

Genomic redistribution of GR monomers and dimers mediates transcriptional response to exogenous glucocorticoid in vivo. Lim, H; Uhlenhaut, NH; Rauch, A; Weiner, J; Huebner, S; Huebner, N; Won, K; Lazar, MA; Tuckermann, J; Steger, DJ. Genome Research. 2015; 25:836-844.

PRDM16 binds MED1 and controls chromatin architecture to determine a brown fat transcriptional program. Harms, MJ; Lim, H; Ho, Y; Shapira, SN; Ishibashi, J; Rajakumari, S; Steger, DJ; Lazar, MA; Won, K; Seale, P. Genes and Development. 2015; 29:298-307.

Anti-diabetic rosiglitazone remodels the adipocyte transcriptome by redistributing transcription to PPARγ-driven enhancers. Step, SE; Lim, H; Marinis, JM; Prokesch, A; Steger, DJ; You, S; Won, K; Lazar, MA. Genes and Development. 2014; 28:1018-1028.

EBF2 determines and maintains brown adipocyte identity. Rajakumari, S; Wu, J; Ishibashi, J; Lim, H; Giang, A; Won, K; Reed, RR; Seale, P. Cell Metabolism. 2013; 17:562-574.

Early B Cell Factor Activity Controls Developmental and Adaptive Thermogenic Gene Programming in Adipocytes. Angueira, AR; Shapira, SN; Ishibashi, J; Sampat, S; Sostre-Colon, J; Emmett, MJ; Titchenell, PM; Lazar, MA; Lim, H; Seale, P. Cell Reports. 2020; 30:2869-2878.e4.

PRDM16 Maintains Homeostasis of the Intestinal Epithelium by Controlling Region-Specific Metabolism. Stine, RR; Sakers, AP; TeSlaa, T; Kissig, M; Stine, ZE; Kwon, CW; Cheng, L; Lim, H; Kaestner, KH; Rabinowitz, JD; et al. Cell Stem Cell. 2019; 25:830-845.e8.

A PRDM16-Driven Metabolic Signal from Adipocytes Regulates Precursor Cell Fate. Wang, W; Ishibashi, J; Trefely, S; Shao, M; Cowan, AJ; Sakers, A; Lim, H; O'Connor, S; Doan, MT; Cohen, P; et al. Cell Metabolism. 2019; 30:174-189.e5.