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Activation of NRG1-ERBB4 signaling potentiates mesenchymal stem cell-mediated myocardial repairs following myocardial infarction.
Liang, X; Ding, Y; Zhang, Y; Chai, Y-H; He, J; Chiu, S-M; Gao, F; Tse, H-F; Lian, Q.
Afiliación
  • Liang X; Department of Medicine, the University of Hong Kong, Hong Kong, China.
  • Ding Y; 1] Department of Medicine, the University of Hong Kong, Hong Kong, China [2] Organ Transplantation Institute, Xiamen University, Fujian Province, China.
  • Zhang Y; Department of Medicine, the University of Hong Kong, Hong Kong, China.
  • Chai YH; 1] Department of Medicine, the University of Hong Kong, Hong Kong, China [2] Organ Transplantation Institute, Xiamen University, Fujian Province, China.
  • He J; Department of Medicine, the University of Hong Kong, Hong Kong, China.
  • Chiu SM; Department of Medicine, the University of Hong Kong, Hong Kong, China.
  • Gao F; Department of Medicine, the University of Hong Kong, Hong Kong, China.
  • Tse HF; 1] Department of Medicine, the University of Hong Kong, Hong Kong, China [2] Research Centre of Heart, Brain, Hormone, and Healthy Aging, Li Ka Shing Faculty of Medicine, the University of Hong Kong, Hong Kong, China [3] Shenzhen Institutes of Research and Innovation, the University of Hong Kong, Ho
  • Lian Q; 1] Department of Medicine, the University of Hong Kong, Hong Kong, China [2] Research Centre of Heart, Brain, Hormone, and Healthy Aging, Li Ka Shing Faculty of Medicine, the University of Hong Kong, Hong Kong, China [3] Shenzhen Institutes of Research and Innovation, the University of Hong Kong, Ho
Cell Death Dis ; 6: e1765, 2015 May 21.
Article en En | MEDLINE | ID: mdl-25996292

Texto completo: 1 Base de datos: MEDLINE Asunto principal: Neurregulina-1 / Células Madre Mesenquimatosas / Receptor ErbB-4 / Infarto del Miocardio Idioma: En Revista: Cell Death Dis Año: 2015 Tipo del documento: Article

Texto completo: 1 Base de datos: MEDLINE Asunto principal: Neurregulina-1 / Células Madre Mesenquimatosas / Receptor ErbB-4 / Infarto del Miocardio Idioma: En Revista: Cell Death Dis Año: 2015 Tipo del documento: Article