Hangzhong Feng, PhD
Research Assistant Professor
Department of Physiology and Biophysics
Contact
Building & Room:
CMWT 512
Office Phone:
Fax:
Lab
Building & Room:
MSB E518
Email:
Related Sites:
About Heading link
The focus of Dr. Feng’s research is to understand the disease mechanism and to find the possible therapeutic target in muscle regulatory proteins of troponin I and troponin T by studying their protein structure-functional relationship in muscle contractions and energy efficiency of cardiac and skeletal muscles. Understanding troponin structures crossing different species, different physiology modifications and different genetic disease mutations helps identify the potential substructure domain of troponin as the effective drug target.
Research/Teaching Heading link
Together with the Jin Lab, Dr. Feng has developed contractility measurements with optimized conditions to evaluate the molecular functional contribution of troponin in muscle contraction at different levels, such as myofilament, single cell, muscle tissue or ex vivo mouse working heart organ level. By integrating our lab research at protein molecular structure and transgenic mice models, we have established the understanding of functional impacts of different troponin structure modifications in physiology or pathology from cardiac and skeletal muscles. Now we are aiming at the troponin micro structure domain of their regulatory conformational change as a future drug target to treat cardiac or skeletal muscle diseases.
Current research projects: 1) Cardiac troponin C-terminal peptide functional effect on cardiac muscle contractility. 2) Slow skeletal muscle troponin T and troponin I mutation in human skeletal muscle nemaline myopathy. 3) Cardiac troponin T and troponin I N-terminal functional role. 4) The Ca2+ buffering role of Tx9 domain in skeletal muscle fast troponin T. 5) The Ca2+ buffering role of 51E domain in cardiac troponin T.
Selected Publications
Feng HZ, Huang X, Jin JP. N-terminal truncated cardiac troponin I enhances Frank-Starling response by increasing myofilament sensitivity to resting tension.J Gen Physiol. 2023 Apr 3;155(4):e202012821. doi: 10.1085/jgp.202012821. Epub 2023 Mar 6.PMID: 36880803
Feng HZ and Jin JP. High efficiency preparation of skinned mouse cardiac muscle strips from cryosections for contractility studies. Exp Physiol. 2020 Nov;105(11):1869-1881. doi: 10.1113/EP088521. Epub 2020 Sep 16
Feng HZ, Jin JP. A protocol to study ex vivo mouse working heart at human-like heart rate. J Mol Cell Cardiol. 2018 Jan; 114:175-184. doi: 10.1016/j.yjmcc.2017.11.011. Epub 2017 Nov 17
Feng HZ, Chen G, Nan C, Huang X, Jin JP. Abnormal splicing in the N-terminal variable region of cardiac troponin T impairs systolic function of the heart with preserved Frank-Starling compensation. Physiol Rep. 2014 Sep 4; 2(9). pii: e12139. doi: 10.14814/phy2.12139. Print 2014 Sep 1
Feng HZ, Biesiadecki BJ, Yu ZB, Hossain MM and Jin JP. Restricted N-terminal truncation of cardiac troponin T: a novel mechanism for functional adaptation to energetic crisis. J. Physiol. (London) 586: 3537-3550, 2008