Xuejun Wang

Summary

Affiliation: University of South Dakota
Country: USA

Publications

  1. ncbi Desmin filaments and cardiac disease: establishing causality
    Xuejun Wang
    Division of Molecular Cardiovascular Biology, Children's Hospital Medical Center, Cincinnati, Ohio, USA
    J Card Fail 8:S287-92. 2002
  2. ncbi AlphaB-crystallin modulates protein aggregation of abnormal desmin
    Xuejun Wang
    Division of Molecular Cardiovascular Biology, Children s Hospital Medical Center, Cincinnati, Ohio, USA
    Circ Res 93:998-1005. 2003
  3. ncbi Enhancement of proteasome function by PA28α overexpression protects against oxidative stress
    Jie Li
    Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, 414 East Clark St, Lee Medical Bldg, Vermillion, SD 57069, USA
    FASEB J 25:883-93. 2011
  4. ncbi Perturbation of cullin deneddylation via conditional Csn8 ablation impairs the ubiquitin-proteasome system and causes cardiomyocyte necrosis and dilated cardiomyopathy in mice
    Huabo Su
    Cardiovascular Research Institute, Sanford School of Medicine of the University of South Dakota, Vermillion, 57069, USA
    Circ Res 108:40-50. 2011
  5. ncbi Protein quality control and degradation in cardiomyocytes
    Xuejun Wang
    Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Vermillion, SD 57069, USA
    J Mol Cell Cardiol 45:11-27. 2008
  6. ncbi Impairment of the ubiquitin-proteasome system in desminopathy mouse hearts
    Jinbao Liu
    Cardiovascular Research Institute, South Dakota Health Research Foundation, University of South Dakota School of Medicine and Sioux Valley Hospitals and Health System, Sioux Falls, South Dakota 57105, USA
    FASEB J 20:362-4. 2006
  7. ncbi In situ dynamically monitoring the proteolytic function of the ubiquitin-proteasome system in cultured cardiac myocytes
    Xin Dong
    Cardiovascular Research Institute, University of South Dakota, Sioux Falls, South Dakota 57105, USA
    Am J Physiol Heart Circ Physiol 287:H1417-25. 2004
  8. ncbi Upregulation of myocardial 11S-activated proteasome in experimental hyperglycemia
    Saul R Powell
    Department of Medicine, The Feinstein Institute for Medical Research and the Albert Einstein College of Medicine, New Hyde Park, NY, USA
    J Mol Cell Cardiol 44:618-21. 2008
  9. ncbi Heart failure and protein quality control
    Xuejun Wang
    Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Vermillion, SD, USA
    Circ Res 99:1315-28. 2006
  10. ncbi GFP reporter mouse models of UPS proteolytic function
    Kristina Lindsten
    FASEB J 20:1027; author reply 1027-8. 2006

Collaborators

  • Jinbao Liu
  • Saul R Powell
  • Jeffrey Saffitz
  • Nico P Dantuma
  • C Patterson
  • Michael Schneider
  • Maria G Masucci
  • Nilanjana Maulik
  • Ruben Mestril
  • Xian Ping Yi
  • Faqian Li
  • A Martin Gerdes
  • Hanqiao Zheng
  • Jie Li
  • Asangi R K Kumarapeli
  • Jibin Zhou
  • Jiaxiang Qu
  • Kathleen M Horak
  • Quanhai Chen
  • Huabo Su
  • Satoru Kobayashi
  • Lu Huber
  • Kristina Lindsten
  • Yi-Da Tang
  • Joseph J Gard
  • Joseph W Glasford
  • Xin Dong
  • Suchithra Menon
  • Asangi R Kumarapeli
  • Ning Wei
  • Baojun Dong
  • Kai Mao
  • Timothy D O'Connell
  • Kelly Graber
  • Qiangrong Liang
  • Lisa M Miller
  • Justin Baker
  • Suleman Said
  • Kiyomi Yamada
  • Brent E Anderson
  • James A Kuzman
  • Jeffrey Robbins
  • Eric F Wawrousek
  • David S Rosenbaum
  • Richard B Schuessler
  • Karen G Green
  • Benjamin C Eloff
  • Kathryn A Yamada
  • Wei Huang
  • Niels R Harden
  • Quan Hai Chen

Detail Information

Publications23

  1. ncbi Desmin filaments and cardiac disease: establishing causality
    Xuejun Wang
    Division of Molecular Cardiovascular Biology, Children's Hospital Medical Center, Cincinnati, Ohio, USA
    J Card Fail 8:S287-92. 2002
    ..CONCLUSIONS: Thus cardiac overexpression of wild-type desmin is not detrimental whereas aberrant aggregation of desmin and disruption of the desmin network remodel the heart and compromise cardiac function...
  2. ncbi AlphaB-crystallin modulates protein aggregation of abnormal desmin
    Xuejun Wang
    Division of Molecular Cardiovascular Biology, Children s Hospital Medical Center, Cincinnati, Ohio, USA
    Circ Res 93:998-1005. 2003
    ..Significantly less aberrant desmin aggregation was observed in the WT-CryAB-overexpressing cells than in the HEK cells. The results suggest that CryAB modulates abnormal desmin aggregation and can serve a cardioprotective role...
  3. ncbi Enhancement of proteasome function by PA28α overexpression protects against oxidative stress
    Jie Li
    Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, 414 East Clark St, Lee Medical Bldg, Vermillion, SD 57069, USA
    FASEB J 25:883-93. 2011
    ....
  4. ncbi Perturbation of cullin deneddylation via conditional Csn8 ablation impairs the ubiquitin-proteasome system and causes cardiomyocyte necrosis and dilated cardiomyopathy in mice
    Huabo Su
    Cardiovascular Research Institute, Sanford School of Medicine of the University of South Dakota, Vermillion, 57069, USA
    Circ Res 108:40-50. 2011
    ..Moreover, the role of CSN in a postmitotic organ and the impact of cardiomyocyte-restricted UPS dysfunction on the heart have not been reported...
  5. ncbi Protein quality control and degradation in cardiomyocytes
    Xuejun Wang
    Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Vermillion, SD 57069, USA
    J Mol Cell Cardiol 45:11-27. 2008
    ..Autophagy may also participate in PQC in cardiomyocytes, especially under pathological conditions. Cardiac PQC often becomes inadequate in heart disease, which may play an important role in the development of congestive heart failure...
  6. ncbi Impairment of the ubiquitin-proteasome system in desminopathy mouse hearts
    Jinbao Liu
    Cardiovascular Research Institute, South Dakota Health Research Foundation, University of South Dakota School of Medicine and Sioux Valley Hospitals and Health System, Sioux Falls, South Dakota 57105, USA
    FASEB J 20:362-4. 2006
    ..Thus, UPS impairment may represent an important pathogenic mechanism underlying cardiac disorders with abnormal protein aggregation...
  7. ncbi In situ dynamically monitoring the proteolytic function of the ubiquitin-proteasome system in cultured cardiac myocytes
    Xin Dong
    Cardiovascular Research Institute, University of South Dakota, Sioux Falls, South Dakota 57105, USA
    Am J Physiol Heart Circ Physiol 287:H1417-25. 2004
    ..Application of this novel system reveals that moderate levels of H2O2, a reactive oxygen species generator, impair proteolytic function of the UPS in cultured cardiac myocytes...
  8. ncbi Upregulation of myocardial 11S-activated proteasome in experimental hyperglycemia
    Saul R Powell
    Department of Medicine, The Feinstein Institute for Medical Research and the Albert Einstein College of Medicine, New Hyde Park, NY, USA
    J Mol Cell Cardiol 44:618-21. 2008
    ..However, 11S-activated proteasome was increased suggesting a response to oxidative protein damage and a potential role for this form of the proteasome in a cardiac pathophysiology...
  9. ncbi Heart failure and protein quality control
    Xuejun Wang
    Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Vermillion, SD, USA
    Circ Res 99:1315-28. 2006
    ..Here, we examine recent data pointing to the importance of protein quality control in cardiac homeostasis and disease...
  10. ncbi GFP reporter mouse models of UPS proteolytic function
    Kristina Lindsten
    FASEB J 20:1027; author reply 1027-8. 2006
  11. ncbi Aberrant protein aggregation is essential for a mutant desmin to impair the proteolytic function of the ubiquitin-proteasome system in cardiomyocytes
    Jinbao Liu
    Cardiovascular Research Institute-South Dakota Health Research Foundation, University of South Dakota School of Medicine and Sioux Valley Hospitals and Health System, Sioux Falls SD 57105, USA
    J Mol Cell Cardiol 40:451-4. 2006
    ..These findings prove for the first time that aberrant protein aggregation is not only sufficient but also required for MT-des to impair UPS proteolytic function in cardiomyocytes...
  12. ncbi Genetic modification of the heart: chaperones and the cytoskeleton
    Asangi R K Kumarapeli
    Cardiovascular Research Institute and Division of Basic Biomedical Sciences, University of South Dakota School of Medicine, 1100 E. 21st Street, Sioux Falls, SD 57105, USA
    J Mol Cell Cardiol 37:1097-109. 2004
    ....
  13. ncbi Intrasarcoplasmic amyloidosis impairs proteolytic function of proteasomes in cardiomyocytes by compromising substrate uptake
    Quanhai Chen
    Cardiovascular Research Institute, South Dakota Health Research Foundation, University of South Dakota School of Medicine, Sioux Valley Hospitals and Health System, Sioux Falls, SD, USA
    Circ Res 97:1018-26. 2005
    ..Because of the central role of the UPS in cell regulation and the high intrasarcoplasmic amyloidosis prevalence in failing human hearts, our data suggest a novel pathogenic process in cardiac disorders with abnormal protein aggregation...
  14. ncbi Remodeling of gap junctions and slow conduction in a mouse model of desmin-related cardiomyopathy
    Joseph J Gard
    Department of Pathology, Box 8118, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Cardiovasc Res 67:539-47. 2005
    ....
  15. ncbi A novel transgenic mouse model reveals deregulation of the ubiquitin-proteasome system in the heart by doxorubicin
    Asangi R K Kumarapeli
    Cardiovascular Research Institute, South Dakota Health Research Foundation, Sioux Falls, South Dakota 57105, USA
    FASEB J 19:2051-3. 2005
    ....
  16. ncbi Nuclear compartmentalization of FAK and FRNK in cardiac myocytes
    Xian Ping Yi
    Cardiovascular Research Institute South Dakota Health Research Foundation, 1100 East 21st Street, Sioux Falls, SD 57105, USA
    Am J Physiol Heart Circ Physiol 290:H2509-15. 2006
    ..These results suggest that FAK and FRNK target different nuclear subdomains by their association with distinct nuclear proteins...
  17. ncbi Subcellular redistribution of focal adhesion kinase and its related nonkinase in hypertrophic myocardium
    Xian Ping Yi
    South Dakota Health Research Foundation Cardiovascular Research Institute, 1400 W 22nd St, Sioux Falls, SD 57105, USA
    Hypertension 41:1317-23. 2003
    ..Serine phosphorylated FAK and FRNK accumulated in membranes and nuclei but not in intercalated disks. Nuclear translocation of FAK and FRNK may play important roles in regulating mechanical signal transduction in cardiac myocytes...
  18. ncbi Structural basis of ventricular remodeling: role of the myocyte
    Faqian Li
    University of South Dakota, 1400 W. 22nd Street, Sioux Falls, SD 57105, USA
    Curr Heart Fail Rep 1:5-8. 2004
    ..Several signaling molecules have been implicated in this process. As we learn more about the components of myocardial remodeling, new strategies to combat the progression of heart disease should arise...
  19. ncbi Cardiac-specific haploinsufficiency of beta-catenin attenuates cardiac hypertrophy but enhances fetal gene expression in response to aortic constriction
    Jiaxiang Qu
    Sanford Research USD, Cardiovascular Research Institute, Sanford School of Medicine of The University of South Dakota and Sanford Health, Sioux Falls, SD 57105, USA
    J Mol Cell Cardiol 43:319-26. 2007
    ..These results suggest that the cytoplasmic level of beta-catenin modulates hypertrophic response and fetal gene reprogramming after pressure overload...
  20. ncbi Diminished GATA4 protein levels contribute to hyperglycemia-induced cardiomyocyte injury
    Satoru Kobayashi
    Cardiovascular Research Institute, Sanford Research, University of South Dakota Sanford School of Medicine, Sioux Falls, SD 57105, USA
    J Biol Chem 282:21945-52. 2007
    ..05), which correlated with increased CHIP mRNA abundance. In summary, increased GATA4 protein degradation may be an important mechanism that contributes to hyperglycemic cardiotoxicity...
  21. ncbi Upregulation of gamma-catenin compensates for the loss of beta-catenin in adult cardiomyocytes
    Jibin Zhou
    Cardiovascular Research Institute, South Dakota Health Research Foundation, 1100 East 21st St, Suite 700, Sioux Falls, SD 57105, USA
    Am J Physiol Heart Circ Physiol 292:H270-6. 2007
    ..The results suggest that upregulation of gamma-catenin can compensate for the loss of beta-catenin in cardiomyocytes to maintain normal cardiac structure and function...
  22. ncbi Low thyroid function leads to cardiac atrophy with chamber dilatation, impaired myocardial blood flow, loss of arterioles, and severe systolic dysfunction
    Yi-Da Tang
    Cardiovascular Research Institute, South Dakota Health Research Foundation, University of South Dakota School of Medicine, Sioux Valley Hospitals and Health Systems, Sioux Falls, SD, USA
    Circulation 112:3122-30. 2005
    ..Hypothyroidism resulted in impaired myocardial blood flow due to a dramatic loss of arterioles. Thus, we have identified 2 important new mechanisms by which low thyroid function may lead to heart failure...
  23. ncbi Myocardial expression and redistribution of GRKs in hypertensive hypertrophy and failure
    Xian Ping Yi
    South Dakota Health Research Foundation Cardiovascular Research Institute, University of South Dakota, 1100 East 21st Street, Sioux Falls, SD 57105, USA
    Anat Rec A Discov Mol Cell Evol Biol 282:13-23. 2005
    ..The increased expression of GRK3 and GRK6 and subcellular redistribution of GRK2, GRK5, and GRK6 in SHHF rats may be involved in abnormal remodeling of cardiac myocytes in hypertensive hypertrophy and failure...