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Taixing Cui
Name:Taixing Cui
Title:Associate Professor
Department:Cell Biology and Anatomy
E-mail:Taixing.Cui@uscmed.sc.edu
Phone: Office: 803-216-3804
Lab: 803-216-3833
Fax: 803-216-3846
Training: MD : 1989 The 4th Military Medical University, P.R. China
PhD: 2001 Ehime University School of Medicine, Japan

Research Focus:

Dr. Cui has a research interest in understanding the nature of cardiac adaptation as well as maladaptive remodeling and dysfunction in diverse pathological settings. In addition, Dr. Cui has a research interest in investigating the source of resident vascular stem cells as well as the role of resident vascular stem cells (VSCs) in vascular regeneration, repair, and lesion formation. Dr. Cui’s laboratory takes multi-disciplinary approaches to explore the key molecules which coordinate the proteasome- and autophagy-dependent protein degradation pathways contributing to cardiac adaptation or dysfunction, as well as to identify the novel determinants in the control of resident VSC generation and resident VSC-mediated vascular repair or lesion formation.

There are four areas of technical strengths in Dr. Cui’s laboratory:

  1. Conventional and inducible cardiomyocyte-restricted genetic manipulation in vivo
  2. Conventional and inducible endothelial cell-, smooth muscle cell-, and adventitial fibroblast-restricted genetic manipulation in vivo
  3. Genetic inducible fate mapping of endothelial cells, vascular smooth muscle cells, adventitial fibroblasts, and resident stem cells in vivo
  4. Cardiovascular physiology analyses in cell, organ and whole animal levels

Two major projects currently underway include:

  1. To identify novel regulators of proteasome- and autophagy-dependent protein quality control in the heart.
  2. To identify the molecular switch of vascular regeneration, repair and lesion formation.

Recent Publications:

  1. Wang X, Cui T*. Autophagy modulation—A potential therapeutic approach in cardiac hypertrophy. Am J Physiol Heart Circ Physiol. 2017 Aug 1;313(2):H304-H319. Invited Review.
  2. Qin Q, Qu C, Niu T, Zang H, Lyu L, Wang X, Nagarkatti M, Nagarkatti P, Janicki JS, Wang XL, Cui T*. Nrf2-mediated cardiac maladaptive remodeling and dysfunction in a setting of autophagy insufficiency. Hypertension. 2016 Jan;67(1):107-17.
  3. Leach DF, Nagarkatti M, Nagarkatti P, Cui T*. Functional states of resident vascular stem cells and vascular remodeling. Front Biol (Beijing). 2015 Oct 1;10(5):387-397. Invited Review.
  4. Lyu L, Wang H, Li B, Qin Q, Qi L, Janicki JS, Nagarkatti M, Nagarkatti P, Janicki JS, Wang XL, Cui T*. A critical role of cardiac fibroblast-derived exosomes in activating renin angiotensin system in cardiomyocytes. J Mol Cell Cardiol. 2015 Dec;89(Pt B):268-79.
  5. Wang H, Lai Y, Mathis BJ, Wang W, Li S, Qu C, Li B, Shao L, Song H, Janicki JS, Sun SC, Wang XL, Tang D, Cui T*. Deubiquitinating enzyme CYLD mediates pressure overload-induced cardiac maladaptive remodeling and dysfunction via downregulating Nrf2. J Mol Cell Cardiol. 2015 Apr 30;84:143-153.
  6. Wang W, Li S, Wang H, Li B, Shao L, Lai Y, Horvath G, Wang Q, Yamamoto M, Janicki JS, Wang XL. Tang D, Cui T*. Nrf2 enhances myocardial clearance of toxic ubiquitinated proteins. J Mol Cell Cardiol. 2014 Jul;72:305-15.
  7. Zhang X, Guo L, Niu T, Shao L, Wu W, Wang W, Lv L, Qin Q, Wang F, Tang D, Wang XL, Cui T*. Ubiquitin carboxyl terminal hydrolyase L1-suppressed autophagic degradation of p21WAF/Cip1 as a novel feedback mechanism in the control of cardiac fibroblast proliferation. PLoS One. 2014 Apr 14;9(4):e94658.
PubMed Link:
http://www.ncbi.nlm.nih.gov/sites/myncbi/1x5hQSoRqx1Qa/bibliography/47465101/public/?sort=date