Zobrazeno 1 - 10
of 13
pro vyhledávání: '"Yuejin Li"'
Autor:
Ping Wan, Kunmei Gong, Li Rougang, Subash C. B. Gopinath, Yuejin Li, Shikui Guo, Yongzhi Wang, Peng Zhang
Publikováno v:
Biotechnology and applied biochemistryReferences. 67(3)
Abdominal aortic aneurysm (AAA) is a serious, life-threatening vascular disease that presents as an enlarged area of the aorta, which is the main artery that carries blood away from the heart. AAA may occur at any location in the aorta, but it is mai
Autor:
Yingjian Liang, Yuejin Li, Tongsen Zheng, Lianxin Liu, Huawen Shi, Boshi Sun, Dalong Yin, Yu Sun, Hongchi Jiang, Shangha Pan, Ruipeng Song, Huanlai Wang, Jing Sun, Jiabei Wang, Tiemin Pei
Publikováno v:
Oncotarget
Yes-associated protein (YAP), a transcriptional co-activator, has important regulatory roles in cell signaling and is dysregulated in a number of cancers. However, the role of YAP in cholangiocarcinoma (CCA) progression remains unclear. Here, we demo
Autor:
Ger J.M. Stienen, Paul J.M. Wijnker, Vasco Sequeira, D. Brian Foster, Yuejin Li, Jolanda van der Velden, Anne M. Murphy, Cristobal G. dos Remedios
Publikováno v:
American Journal of Physiology. Heart and Circulatory Physiology, 306(8), H1171-H1181. American Physiological Society
Wijnker, P J M, Sequeira Oliveira, V, Foster, D B, Li, Y J, dos Remedios, C G, Murphy, A M, Stienen, G J M & van der Velden, J 2014, ' Length-dependent activation is modulated by cardiac troponin I bisphosphorylation at Ser23 and Ser24 but not by Thr143 phosphorylation ', American Journal of Physiology. Heart and Circulatory Physiology, vol. 306, no. 8, pp. H1171-H1181 . https://doi.org/10.1152/ajpheart.00580.2013
Wijnker, P J M, Sequeira Oliveira, V, Foster, D B, Li, Y J, dos Remedios, C G, Murphy, A M, Stienen, G J M & van der Velden, J 2014, ' Length-dependent activation is modulated by cardiac troponin I bisphosphorylation at Ser23 and Ser24 but not by Thr143 phosphorylation ', American Journal of Physiology. Heart and Circulatory Physiology, vol. 306, no. 8, pp. H1171-H1181 . https://doi.org/10.1152/ajpheart.00580.2013
Frank-Starling's law reflects the ability of the heart to adjust the force of its contraction to changes in ventricular filling, a property based on length-dependent myofilament activation (LDA). The threonine at amino acid 143 of cardiac troponin I
Autor:
Changlong Nan, Guozhen Chen, Yuejin Li, Jian Ping Jin, Jie Tian, Pierre Yves Jean-Charles, Ira J. Gelb, Xupei Huang, Lei Zhang
Publikováno v:
Journal of Molecular and Cellular Cardiology. 62:227-236
Our aim was to explore the dose-dependent diastolic dysfunction and the mechanisms of heart failure and early death in transgenic (TG) mice modeling human restrictive cardiomyopathy (RCM). The first RCM mouse model (cTnI(193His) mice) carrying cardia
Autor:
Yuejin Li, Guangshuo Zhu, Cyrus Takahashi, Djahida Bedja, Genaro Ramirez-Correa, Nazareno Paolocci, David A Kass, Anne M Murphy
Publikováno v:
Circulation. 132
Background: Phosphorylation of cardiac troponin I (cTnI) on Ser199 is significantly increased in human heart failure (HF), however its cardiac impact in vivo remains unknown. In addition, selective proteolysis of cTnI is a marker of myocardial injury
Autor:
Yuejin Li, Jennifer E. Van Eyk, Cris dos Remedios, Anne M. Murphy, Pingbo Zhang, Ger J.M. Stienen, Paul J.M. Wijnker, Jolanda van der Velden, D. Brian Foster
Publikováno v:
Wijnker, P J M, Li, Y, Zhang, P, Foster, D B, dos Remedios, C, van Eyk, J E, Stienen, G J M, Murphy, A M & van der Velden, J 2015, ' A novel phosphorylation site, Serine 199, in the C-terminus of cardiac troponin I regulates calcium sensitivity and susceptibility to calpain-induced proteolysis ', Journal of Molecular and Cellular Cardiology, vol. 82, pp. 93-103 . https://doi.org/10.1016/j.yjmcc.2015.03.006
Journal of Molecular and Cellular Cardiology, 82, 93-103. Academic Press Inc.
Journal of Molecular and Cellular Cardiology, 82, 93-103. Academic Press Inc.
Phosphorylation of cardiac troponin I (cTnI) by protein kinase C (PKC) is implicated in cardiac dysfunction. Recently, Serine 199 (Ser199) was identified as a target for PKC phosphorylation and increased Ser199 phosphorylation occurs in end-stage fai
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e3559c7e7ce9d68ead4aa3b34849d1be
https://research.vumc.nl/en/publications/c2adab85-4fc9-45f8-ba06-bf15b53fdc50
https://research.vumc.nl/en/publications/c2adab85-4fc9-45f8-ba06-bf15b53fdc50
Autor:
J.-P. Jin, Yuejin Li, Changlong Nan, Pierre-Yves Jean-Charles, Xupei Huang, L. Zhang, Nariman Gobara, J. Tian, Guozhen Chen
Publikováno v:
Biochemistry Research International
Biochemistry Research International, Vol 2012 (2012)
Biochemistry Research International, Vol 2012 (2012)
Cardiomyopathies are common cardiac disorders that primarily affect cardiac muscle resulting in cardiac dysfunction and heart failure. Transgenic mouse disease models have been developed to investigate the cellular mechanisms underlying heart failure
Autor:
J.-P. Jin, Han-Zhong Feng, Pierre-Yves Jean-Charles, Changlong Nan, Guozheng Chen, Yuejin Li, Xupei Huang
Publikováno v:
Biophysical Journal. 100(3)
Our previous studies have demonstrated that the phenotype of the transgenic mouse hearts expressing a restrictive cardiomyopathy (RCM) cardiac troponin I (cTnI) C-terminal mutation (R193H) is characterized by a diastolic dysfunction and sudden cardia
Autor:
Yingcai Wang, Han Zhong Feng, Gang Wu, Pierre Yves Jean Charles, Jose R. Pinto, Jian Ping Jin, Jie Tian, Yuejin Li, Xupei Huang, Jingsheng Liang, Changlong Nan, James D. Potter
Publikováno v:
Journal of molecular and cellular cardiology. 49(3)
Several cardiac troponin I (cTnI) mutations are associated with restrictive cardiomyopathy (RCM) in humans. We have created transgenic mice (cTnI(193His) mice) that express the corresponding human RCM R192H mutation. Phenotype of this RCM animal mode
Publikováno v:
Circulation. 118
Multiple mutations in cardiac troponin I (cTnI) have been linked to the development of restrictive cardiomyopathy (RCM) in human patients. Among them, K178E mutation has the worst clinical phenotype. K178E mutation may influence the inhibitory functi