Wu LAB

Dr. Tongbin Wu is dedicated to the study of left ventricular noncompaction (LVNC) and dilated cardiomyopathy (DCM). Using genetics, next-generation sequencing tools and molecular biology, his work aims to understand LVNC and DCM during embryonic development to prevent congenital heart disease and to improve the treatment and diagnosis of patients worldwide. Dr. Wu’s goal is to gain a deeper understanding of these networks, paving the way for the identification of novel therapeutic targets and the development of more effective treatments not only for LVNC but also for other heart diseases.

News From The Wu Lab

Dr. Tongbin Wu, heart disease researcher, discovered key proteins in major study

Tongbin Wu, Ph.D. Publishes Major Study Uncovering Key Proteins that Keep the Heart Beating Properly

A groundbreaking new study led by researchers at the Masonic Medical Research Institute (MMRI) has identified that two closely related proteins, RBPMS and RBPMS2, act in tandem to protect the heart’s ability to process the genetic information needed for normal heart development and function.

Read more here.

Areas of Investigation

Transcriptional regulation in heart development and disease: According to the "Central Dogma”, genetic information flows from DNA to RNA, and then from RNA to protein. As the initial step, transcription is the process of copying a segment of DNA, known as “gene”, into RNA. Transcription regulation determines when and where genes are expressed, influencing the production of proteins, which are indispensable for nearly all biological processes in our body. Transcription regulation profoundly affects the development and function of our body. In the Wu laboratory, we focus on studying transcription factors – proteins regulate transcription – whose malfunction often leads to LVNC and other heart diseases. Understanding the molecular mechanisms by which these transcription factors regulate gene expression during heart development, and how their dysfunction leads to disease, will contribute to the development of innovative therapies in the future.

Post-transcriptional regulation in heart development and disease:  Following transcription from DNA, the initial RNA form is known as precursor messenger RNA (pre-mRNA). Pre-mRNA undergoes various post-transcriptional processing or modifications to mature into messenger RNA (mRNA), which serves as the template for protein synthesis. Often mediated by RNA-binding proteins (RBPs), post-transcriptional regulation significantly influences the composition and function of proteins, making it pivotal for the development and function of our body. Built on Dr. Wu’s expertise in RNA biology and cardiovascular medicine, the other major focus of our group is post-transcription regulation by RBPs that are mutated or dysregulated in heart diseases. Utilizing a range of genetic and genomic research tools, our aim is to decipher the intricate gene regulation network within the heart. By doing so, we can identify potential drug targets and devise innovative therapeutic approaches.

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Lab Focus

Genetics

tongbin wu testing in a lab

The Wu lab employs models to study heart diseases. Using CRISPR-Cas9 technology, genetic mutations or deletions identified in humans are introduced into the genome, allowing for the observation of disease phenotypes. These models serve as valuable tools for elucidating the molecular mechanisms underlying heart diseases and for conducting pre-clinical testing of potential therapeutic interventions.

Genomics

The Wu lab employs multi-omics genomic approaches to unravel the gene regulation network within the heart. Specifically, bulk or single-cell RNA sequencing (RNA-seq) and spatial gene expression technology are utilized to analyze spatiotemporal gene expression changes during development or under diseased conditions (transcriptomics). Mass spectrometry is employed to investigate protein expression alterations (proteomics) and map out protein interaction networks (interactome). Chromatin immunoprecipitation followed by sequencing (ChIP-seq) is used to pinpoint the binding locations of transcription factors on the genome (epigenomics), while crosslinking and immunoprecipitation followed by sequencing (CLIP-seq) is applied to determine the locations where RNA binding proteins occupy on the RNA (transcriptomics). The integration of information obtained from these techniques provides insights into how gene expression is regulated transcriptionally and post-transcriptionally in the heart at the molecular level.

testing in lab

Molecular & Cell biology

Tech in a lab running experiments

Our lab performs routine molecular and cell biology techniques as the basis for all our research, including polymerase chain reaction (PCR), gel electrophoresis, western blot, immunofluorescence, primary cell cultures, cell line cultures, and more.

Tongbin Wu headshot

Meet Dr. Tongbin Wu

Assistant Professor of Biomedical Research and Translational Medicine

tongbinwu@mmri.edu

Wu completed his Ph.D. in biochemistry and molecular biology at Wuhan University, Wuhan, China, and his postdoctoral training in molecular cardiology at the University of California San Diego (UCSD), San Diego, California. While at UCSD, Wu’s work was published in highly regarded scientific journals including, Circulation, PNAS, Circulation Research, PLOS Genetics and Nature Structure and Molecular Biology.

Lab Members

Chao Gao headshot

Chao Gao, M.D.

Postdoctoral Fellow

Gao holds a M.D. degree from China Medical University, Shenyang, China, and she is finishing her Ph.D. degree from University of South Carolina School of Medicine, Columbia, South Carolina, in May, 2025. Her studies have been in vascular and cardiovascular research.

Elise Stanley headshot

Elise Stanley

Research Assistant

Stanley holds a bachelor's degree in chemistry from Johns Hopkins University, Baltimore, Maryland. Stanley joined MMRI in 2024 with a focus on RBPMS, a vital RNA-binding protein within cardiomyocytes.

Past Members

Zizhen Liu, 2023-2024
Zhijie Han, Summer 2024
Reaghan Sassower, Summer 2024
Enxu Li, Ph.D. 2024-2025
Victoria Cioni, Summer 2025

Publications

  1. Zhang, Z, Wu, T, Chen, Z, Chen, D, Liang, Z, Adams, C et al.. Transcriptional Readthrough at Atf4 Locus Suppresses Rps19bp1 and Impairs Heart Development. bioRxiv. 2025; :. doi: 10.1101/2025.08.26.672495. PubMed PMID:40909608 PubMed Central PMC12407945.
  2. Wu, T, Chen, Z, Gao, C, Stanley, EV, Zhang, Z, Gu, Y et al.. RBPMS and RBPMS2 Cooperate to Safeguard Cardiac Splicing. Circ Res. 2025;137 (7):1027-1044. doi: 10.1161/CIRCRESAHA.125.326948. PubMed PMID:40859824 .
  3. Wu, T, Chen, Z, Zhang, Z, Zhou, X, Gu, Y, Dinenno, FA et al.. RBPMS and RBPMS2 Cooperate to Safeguard Cardiac Splicing. bioRxiv. 2024; :. doi: 10.1101/2024.11.07.622565. PubMed PMID:39574760 PubMed Central PMC11581027.
  4. Zhou, X, Fang, X, Ithychanda, SS, Wu, T, Gu, Y, Chen, C et al.. Interaction of Filamin C With Actin Is Essential for Cardiac Development and Function. Circ Res. 2023;133 (5):400-411. doi: 10.1161/CIRCRESAHA.123.322750. PubMed PMID:37492967 PubMed Central PMC10529502.
  5. Wu, T, Xu, Y, Zhang, L, Liang, Z, Zhou, X, Evans, SM et al.. Filamin C is Essential for mammalian myocardial integrity. PLoS Genet. 2023;19 (1):e1010630. doi: 10.1371/journal.pgen.1010630. PubMed PMID:36706168 PubMed Central PMC9907827.
  6. Bogomolovas, J, Zhang, Z, Wu, T, Chen, J. Automated quantification and statistical assessment of proliferating cardiomyocyte rates in embryonic hearts. Am J Physiol Heart Circ Physiol. 2023;324 (3):H288-H292. doi: 10.1152/ajpheart.00483.2022. PubMed PMID:36563012 PubMed Central PMC9886340.
  7. Wu, T, Liang, Z, Zhang, Z, Liu, C, Zhang, L, Gu, Y et al.. PRDM16 Is a Compact Myocardium-Enriched Transcription Factor Required to Maintain Compact Myocardial Cardiomyocyte Identity in Left Ventricle. Circulation. 2022;145 (8):586-602. doi: 10.1161/CIRCULATIONAHA.121.056666. PubMed PMID:34915728 PubMed Central PMC8860879.
  8. Wu, T, Chen, J. p38 MAPK reins in right ventricular growth. J Clin Invest. 2020;130 (10):5109-5111. doi: 10.1172/JCI140793. PubMed PMID:32865520 PubMed Central PMC7524502.
  9. Liu, C, Spinozzi, S, Feng, W, Chen, Z, Zhang, L, Zhu, S et al.. Homozygous G650del nexilin variant causes cardiomyopathy in mice. JCI Insight. 2020;5 (16):. doi: 10.1172/jci.insight.138780. PubMed PMID:32814711 PubMed Central PMC7455123.
  10. Mu, Y, Yu, H, Wu, T, Zhang, J, Evans, SM, Chen, J et al.. O-linked β-N-acetylglucosamine transferase plays an essential role in heart development through regulating angiopoietin-1. PLoS Genet. 2020;16 (4):e1008730. doi: 10.1371/journal.pgen.1008730. PubMed PMID:32251422 PubMed Central PMC7182263.
  11. Liu, C, Spinozzi, S, Chen, JY, Fang, X, Feng, W, Perkins, G et al.. Nexilin Is a New Component of Junctional Membrane Complexes Required for Cardiac T-Tubule Formation. Circulation. 2019;140 (1):55-66. doi: 10.1161/CIRCULATIONAHA.119.039751. PubMed PMID:30982350 PubMed Central PMC6889818.
  12. Wu, T, Mu, Y, Bogomolovas, J, Fang, X, Veevers, J, Nowak, RB et al.. HSPB7 is indispensable for heart development by modulating actin filament assembly. Proc Natl Acad Sci U S A. 2017;114 (45):11956-11961. doi: 10.1073/pnas.1713763114. PubMed PMID:29078393 PubMed Central PMC5692592.
  13. Fang, X, Bogomolovas, J, Wu, T, Zhang, W, Liu, C, Veevers, J et al.. Loss-of-function mutations in co-chaperone BAG3 destabilize small HSPs and cause cardiomyopathy. J Clin Invest. 2017;127 (8):3189-3200. doi: 10.1172/JCI94310. PubMed PMID:28737513 PubMed Central PMC5531406.
  14. Fang, X, Stroud, MJ, Ouyang, K, Fang, L, Zhang, J, Dalton, ND et al.. Adipocyte-specific loss of PPARγ attenuates cardiac hypertrophy. JCI Insight. 2016;1 (16):e89908. doi: 10.1172/jci.insight.89908. PubMed PMID:27734035 PubMed Central PMC5053146.
  15. Shimoda, Y, Matsuo, K, Kitamura, Y, Ono, K, Ueyama, T, Matoba, S et al.. Diabetes-Related Ankyrin Repeat Protein (DARP/Ankrd23) Modifies Glucose Homeostasis by Modulating AMPK Activity in Skeletal Muscle. PLoS One. 2015;10 (9):e0138624. doi: 10.1371/journal.pone.0138624. PubMed PMID:26398569 PubMed Central PMC4580461.
  16. Wu, T, Fu, XD. Genomic functions of U2AF in constitutive and regulated splicing. RNA Biol. 2015;12 (5):479-85. doi: 10.1080/15476286.2015.1020272. PubMed PMID:25901584 PubMed Central PMC4615725.
  17. Shao, C, Yang, B, Wu, T, Huang, J, Tang, P, Zhou, Y et al.. Mechanisms for U2AF to define 3' splice sites and regulate alternative splicing in the human genome. Nat Struct Mol Biol. 2014;21 (11):997-1005. doi: 10.1038/nsmb.2906. PubMed PMID:25326705 PubMed Central PMC4429597.
  18. Domenighetti, AA, Chu, PH, Wu, T, Sheikh, F, Gokhin, DS, Guo, LT et al.. Loss of FHL1 induces an age-dependent skeletal muscle myopathy associated with myofibrillar and intermyofibrillar disorganization in mice. Hum Mol Genet. 2014;23 (1):209-25. doi: 10.1093/hmg/ddt412. PubMed PMID:23975679 PubMed Central PMC3916749.
  19. Xue, Y, Zhou, Y, Wu, T, Zhu, T, Ji, X, Kwon, YS et al.. Genome-wide analysis of PTB-RNA interactions reveals a strategy used by the general splicing repressor to modulate exon inclusion or skipping. Mol Cell. 2009;36 (6):996-1006. doi: 10.1016/j.molcel.2009.12.003. PubMed PMID:20064465 PubMed Central PMC2807993.
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Chase Kessinger, Ph.D.

Chase Kessinger, Ph.D.

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Chase Kessinger, Ph.D.

Chase Kessinger, Ph.D.