The α-like scorpion toxin BmK I enhances membrane excitability via persistent sodium current by preventing slow inactivation and deactivation of rNav1.2a expressed in Xenopus Oocytes

Toxicology in Vitro

Volumn 23, Issue 4, 2009, Pages 561-568

  Zhu, Mang Mang ^a   Tan, Miao ^a   Cheng, Hui Wen ^b   Ji, Yong Hua ^b  

^a UNIVERSITY OF CHINESE ACADEMY OF SCIENCES   (China)

^b SHANGHAI UNIVERSITY   (China)

Author keywords

Like toxin; Deactivation; Membrane excitability; Nav1.2; Persistent sodium current; Slow inactivation

Indexed keywords

BMK I TOXIN; NEUROTOXIN; SODIUM CHANNEL; UNCLASSIFIED DRUG;

ANIMAL CELL; ARTICLE; CELL MEMBRANE DEPOLARIZATION; CONCENTRATION RESPONSE; ELECTRIC POTENTIAL; ELECTRODE; ENZYME ACTIVATION; ENZYME INACTIVATION; EPILEPSY; FEMALE; MEMBRANE POTENTIAL; NERVE EXCITABILITY; NONHUMAN; OOCYTE; PROTEIN EXPRESSION; SCORPION; SODIUM CURRENT; XENOPUS;

ANIMALS; FEMALE; MEMBRANE POTENTIALS; OOCYTES; RATS; SCORPION VENOMS; SODIUM CHANNELS; XENOPUS LAEVIS;

RATTUS; SCORPIONES;

EID: 67349272291     PISSN: 08872333     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.tiv.2008.12.022     Document Type: Article

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