Number of items: 4.
Article
    Alharbi, H. O., Hardyman, M. A., Cull, J. J., Markou, T., Cooper, S. T. E., Glennon, P. E., Fuller, S. J., Sugden, P. H. and Clerk, A.  ORCID: https://orcid.org/0000-0002-5658-0708
  
(2022)
Cardiomyocyte BRAF is a key signalling intermediate in cardiac hypertrophy in mice.
    Clinical Science, 136 (22).
    
         pp. 1661-1681.
      
     ISSN 0143-5221
  
doi: 10.1042/CS20220607
ORCID: https://orcid.org/0000-0002-5658-0708
  
(2022)
Cardiomyocyte BRAF is a key signalling intermediate in cardiac hypertrophy in mice.
    Clinical Science, 136 (22).
    
         pp. 1661-1681.
      
     ISSN 0143-5221
  
doi: 10.1042/CS20220607
  
    Clerk, A.  ORCID: https://orcid.org/0000-0002-5658-0708, Meijles, D. N., Hardyman, M. A., Fuller, S. J., Chothani, S. P., Cull, J. J., Cooper, S. T. E., Alharbi, H. O., Vanezis, K., Felkin, L. E., Markou, T., Leonard, S. J., Shaw, S. W., Rackham, O. J. L., Cook, S. A., Glennon, P. E., Sheppard, M. N., Sembrat, J. C., Rojas, M., McTiernan, C. F., Barton, P. J. and Sugden, P. H.
  
(2022)
Cardiomyocyte BRAF and type 1 RAF inhibitors promote cardiomyocyte and cardiac hypertrophy in mice in vivo.
    Biochemical Journal, 479 (3).
    
         pp. 401-424.
      
     ISSN 0264-6021
  
doi: 10.1042/BCJ20210615
ORCID: https://orcid.org/0000-0002-5658-0708, Meijles, D. N., Hardyman, M. A., Fuller, S. J., Chothani, S. P., Cull, J. J., Cooper, S. T. E., Alharbi, H. O., Vanezis, K., Felkin, L. E., Markou, T., Leonard, S. J., Shaw, S. W., Rackham, O. J. L., Cook, S. A., Glennon, P. E., Sheppard, M. N., Sembrat, J. C., Rojas, M., McTiernan, C. F., Barton, P. J. and Sugden, P. H.
  
(2022)
Cardiomyocyte BRAF and type 1 RAF inhibitors promote cardiomyocyte and cardiac hypertrophy in mice in vivo.
    Biochemical Journal, 479 (3).
    
         pp. 401-424.
      
     ISSN 0264-6021
  
doi: 10.1042/BCJ20210615
  
    Meijles, D. N., Cull, J. J., Cooper, S. T. E., Markou, T., Hardyman, M. A., Fuller, S. J., Alharbi, H. O., Haines, Z. H. R., Alcantara Alonso, V.  ORCID: https://orcid.org/0000-0002-9782-2398, Glennon, P. E., Sheppard, M. N., Sugden, P. H. and Clerk, A.
ORCID: https://orcid.org/0000-0002-9782-2398, Glennon, P. E., Sheppard, M. N., Sugden, P. H. and Clerk, A.  ORCID: https://orcid.org/0000-0002-5658-0708
  
(2021)
The anti-cancer drug dabrafenib is not cardiotoxic and inhibits cardiac remodelling and fibrosis in a murine model of hypertension.
    Clinical Science, 135 (14).
    
         pp. 1631-1647.
      
     ISSN 0143-5221
  
doi: 10.1042/CS20210192
ORCID: https://orcid.org/0000-0002-5658-0708
  
(2021)
The anti-cancer drug dabrafenib is not cardiotoxic and inhibits cardiac remodelling and fibrosis in a murine model of hypertension.
    Clinical Science, 135 (14).
    
         pp. 1631-1647.
      
     ISSN 0143-5221
  
doi: 10.1042/CS20210192
  
    Meijles, D. N., Zoumpoulidou, G., Markou, T., Rostron, K. A., Patel, R., Lay, K., Handa, B. S., Wong, B., Sugden, P. H. and Clerk, A.  ORCID: https://orcid.org/0000-0002-5658-0708
  
(2019)
The cardiomyocyte "redox rheostat": Redox signalling via the AMPK-mTOR axis and regulation of gene and protein expression balancing survival and death.
    Journal of molecular and cellular cardiology, 129.
    
         pp. 118-129.
      
     ISSN 1095-8584
  
doi: 10.1016/j.yjmcc.2019.02.006
ORCID: https://orcid.org/0000-0002-5658-0708
  
(2019)
The cardiomyocyte "redox rheostat": Redox signalling via the AMPK-mTOR axis and regulation of gene and protein expression balancing survival and death.
    Journal of molecular and cellular cardiology, 129.
    
         pp. 118-129.
      
     ISSN 1095-8584
  
doi: 10.1016/j.yjmcc.2019.02.006
  
This list was generated on Thu Oct 30 23:34:58 2025 UTC.