Jian-Ping Jin, MD, PhD
Professor
Associate Head for Research
Department of Physiology and Biophysics
Contact
Building & Room:
CMWT 508
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Building & Room:
MSB E518
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About
After his medical training in China and graduate education at University of Iowa, Dr. Jin completed residency in cardiovascular medicine and postdoctoral research fellowships at University of Texas at Austin and University of Alberta, Canada. He was Assistant Professor of Biochemistry and Molecular Biology at University of Calgary, Canada, Associate Professor of Physiology and Biophysics with Tenure at Case Western Reserve University, Section Chief of Molecular Cardiology at ENH Research Institute and Professor of Medicine with Tenure at Northwestern University Feinberg School of Medicine, and William D. Traitel Endowed Professor with tenure and Chairman of the Department of Physiology at Wayne State University. Dr. Jin joined the Department of Physiology and Biophysics at UIC as a tenured professor in December 2020.
Dr. Jin is a leading researcher in the field of muscle contractility and cell motility. Dr. Jin has published 190+ research papers and 30+ review articles in international journals and was Editor-in-Chief for the journal Archives of Biochemistry and Biophysics from 2012 to 2025. He has served on various journal and grant review panels and lectured at numerous national and international venues. Dr. Jin’s current research interest is in the evolution, gene regulation, structure-function relationship and pathophysiological adaptations of cytoskeleton and muscle contractile proteins.
Originated from his scientific research, some of Dr. Jin’s discoveries have led to translational applications in the diagnosis of myocardial infarction, and the treatment of heart failure and cancer metastasis as described in 7 issued and 3 pending US and international patents, of which he is the inventor.
Research/Teaching
Established in 1993, Dr. Jin’s laboratory has been working on the regulation and structure-function relationships of contractile and cytoskeleton proteins, especially the actin thin filament regulatory proteins troponin and calponin in muscle and non-muscle cells.
Muscle (cardiac, skeletal and smooth) contraction and non-muscle cell motility play vital roles in physiological activities and pathological conditions. Focusing on the structure-function relationships of troponin and calponin, Dr. Jin’s research uses genetic and molecular engineering to investigate protein isoform evolution and expression as well as posttranslational modifications. Biochemical, biophysical, immunochemical and cell biological methods are employed in protein structural and functional determinations. Cell culture systems and transgenic/gene knock-out/knock-in mouse models are developed for integrative characterization of physiological and pathophysiological significance at cellular, organ and whole animal levels. Based on structure-function relationship data, protein and peptide constructs are designed for functional characterization and therapeutic development.
On going projects:
a) Post-translational regulation of troponin structure and function in cardiac and skeletal muscles and development therapeutic peptides: Restrictive proteolytic modifications of cardiac troponin I and troponin T are studied for functional impacts on Ca(2+)-regulation of myocardial contraction and relaxation in adaptation to hemodynamic stresses and heart failure. Conformationally modulated sub-molecular structures are identified and characterized to derive peptide reagents for therapeutic applications and drug screening.
b) Mechanistic insights of troponin T-tropomyosin interactions in the kinetics of muscle contraction and relaxation: The functional impacts of troponin T mutations that impairs tropomyosin-binding sites and overall conformation are characterized to understand the functions of the three tropomyosin binding sites in the Ca(2+)-regulation of cardiac and skeletal muscle contraction and relaxation underlying myopathic phenotypes. The studies are aimed to develop therapeutic approaches for improving contractile efficiency and the treatment of heart failure and skeletal muscle weaknesses.
c) Mechanical tension regulation and function of calponin and transgelin: To study physiological functions of the calponin family proteins as troponin analogs in smooth muscle contractility and non-muscle cell motility during cytokinesis, cell migration, inflammation, and fibrotic and calcific tissue remodeling, the research is focused on static mechanical tension regulated calponin and SM22 gene expression and protein degradation in epithelial, endothelial, fibroblast, macrophages and smooth muscle cells in various pathological conditions especially inflammatory diseases.
d) Immunological detection of biomarkers: Peptide-specific monoclonal antibodies are used to develop new diagnostic tests for myocardial and infectious diseases.
Dr. Jin participates in the teaching of several muscle, cell motility and biotechnology related courses.
Selected Publications
Li, Q., Feng, H.-F., Jin, J.-P. (2026) Thin filament interaction and Ca2+-desensitization effect of the C-terminal end peptide of cardiac troponin T and loss of function in hypertrophic cardiomyopathy mutants. J Mol Cell Cardiol. In press.
Cao, T., Feng, H.-Z., Jayasundar, J.J., Jin, J.-P. (2025) The Highly Conserved C-terminal End Segment of Troponin T Binds Tropomyosin and Actin to Function in Modulating Contractile Kinetics. Proc Natl Acad Sci, 122(27):e2507107122.
Feng, H.-Z., Strauss K.A., Jin, J.-P. (2025) Potential cytotoxicity of truncated slow skeletal muscle troponin T in a loss of function TNNT1 myopathy mouse model. FEBS J. 292(20):5525-5539.
J.-P. Jin and Qi-Quan Huang (2025) Calponin and Transgelin: Molecular Evolution, Function, Regulation and Medical Relevance. Nova Science Publishers.
Hsieh, T.-B., Jin, J.-P. (2024) Loss of Calponin 2 Causes Premature Ovarian Insufficiency in Mice. J. Ovarian Res. 7(1):37. doi: 10.1186/s13048-024-01346-y
Rasmussen, M., Jin, J.-P. (2024) Mechanoregulation and Function of Calponin and Transgelin. Biophysics Reviews. 5(1):011302. doi: 10.1063/5.0176784
Feng, H.-Z., Huang, X, Jin, J.-P. (2023) N-terminal truncated cardiac troponin I enhances Frank-Starling response by increasing myofilament sensitivity to resting tension. J. Gen. Physiol. 155(4):e202012821.
Hsieh, T.-B., Jin, J.-P. (2023) Evolution and Function of Calponin and Transgelin. Frontiers Cell Dev Biol. 11:1206147. doi: 10.3389/fcell.2023.1206147.
Hsieh, J.T.-B., Jin J.-P. (2022) Loss of Calponin 2 Causes Age-Progressive Proteinuria in Mice. Physiol. Rep. 10(18):e15370. doi: 10.14814/phy2.15370.
Hsieh, J.T.-B., Feng, H.-Z., Jin J.-P. (2022) Deletion of Calponin 2 Reduces Post-surgery Peritoneal Adhesion. J. Invest. Surgery. 35:517-524.
Rasmussen, M., Feng, H.-Z., Jin, J.-P. (2022) Evolution of the N-terminal regulation of cardiac troponin I for heart function of tetrapods: Lungfish presents an example of the emergence of novel submolecular structure to lead the capacity of adaptation. J. Mol. Evol. 90:30-43.
Qian, A. Hsieh, J.T.-B., Hossain, M.M., J. J.-C. Lin, Jin J.-P. (2021) A Rapid Degradation of Calponin 2 Is Required for Cytokinesis. Am J Physiol Cell Physiol. 321:C355-C368.
Rasmussen, M., Jin, J.-P. (2021) Troponin Variants as Markers of Skeletal Muscle Health and Diseases. Frontiers Striated Muscle Physiol. 12:747214.
Hornos, F., Feng, H.-Z., Rizzuti, B., Palomino-Schätzlein, M., Neira, J.L. , Jin, J.-P. (2021) The isolated C-terminal peptide of troponin I populates a nascent-helix as a basis for binding tropomyosin at micromolar affinity to produce myofilament Ca2+-desensitization. J. Biol. Chem. 296:100228. doi: 10.1074/jbc.RA120.016012.
Cao, T., Sujkowski, A., Cobb, T., Wessells, R.J., Jin, J.-P. (2020) The glutamic acid-rich long C-terminal extension of troponin T has a critical role in insect muscle functions. J. Biol. Chem. 295:3794-3807.
Feng, H.-Z., Jin, J.-P. (2020) High Efficiency Preparation of Skinned Mouse Cardiac Muscle Strips from Cryosections for Myofilament Contractility Studies. J. Exp. Physiol. 28:10.1113/EP088521.
Wong, S., Feng, H.-Z., Jin, J.-P. (2019) The Evolutionarily Conserved C-Terminal Peptide of Troponin I Is An Independently Folded Regulatory Structure and Can Function as A Myofilament Ca2+-Desensitizer. J. Mol. Cell. Cardiol. 136:42-52.