RhoA S-nitrosylation as a regulatory mechanism influencing endothelial barrier function in response to G(+)-bacterial toxins Article

Chen, F, Wang, Y, Rafikov, R et al. (2017). RhoA S-nitrosylation as a regulatory mechanism influencing endothelial barrier function in response to G(+)-bacterial toxins . BIOCHEMICAL PHARMACOLOGY, 127 34-45. 10.1016/j.bcp.2016.12.014

Open Access International Collaboration

cited authors

  • Chen, F; Wang, Y; Rafikov, R; Haigh, S; Zhi, WB; Kumar, S; Doulias, PT; Rafikova, O; Pillich, H; Chakraborty, T; Lucas, R; Verin, AD; Catravas, JD; She, JX; Black, SM; Fulton, DJR

sustainable development goals

authors

publication date

  • March 1, 2017

webpage

published in

keywords

  • ACTIVATION
  • DENITROSYLATION
  • Endothelial
  • G(+)-toxins
  • KINASE-C-ALPHA
  • LUNG INJURY
  • Life Sciences & Biomedicine
  • NITRIC-OXIDE
  • NITROSATION
  • NO
  • Nitric oxide
  • OXIDE-INDUCED INHIBITION
  • Permeability
  • Pharmacology & Pharmacy
  • RESPIRATORY-DISTRESS-SYNDROME
  • RYANODINE RECEPTOR
  • RhoA
  • S-nitrosylation
  • Science & Technology

Digital Object Identifier (DOI)

publisher

  • PERGAMON-ELSEVIER SCIENCE LTD

start page

  • 34

end page

  • 45

volume

  • 127