R. R. Cassulini

A proteomic analysis of the early secondary molecular effects caused by Cn2 scorpion toxin on neuroblastoma cells.

Miguel Rios, L. Possani, F. Coronas, 2014, Journal of proteomics.

Binding Specificity of Sea Anemone Toxins to Nav 1.1-1.6 Sodium Channels

Enzo Wanke, Jeffrey J Clare, E. Redaelli, 2004, Journal of Biological Chemistry.

Modulatory Proteins Can Rescue a Trafficking Defective Epileptogenic Nav1.1 Na+ Channel Mutant

S. Franceschetti, E. Wanke, A. Gambardella, 2007, The Journal of Neuroscience.

Electroclinical Features of a Family with Simple Febrile Seizures and Temporal Lobe Epilepsy Associated with SCN1A Loss‐of‐Function Mutation

S. Franceschetti, E. Wanke, A. Quattrone, 2007, Epilepsia.

A large number of novel Ergtoxin‐like genes and ERG K+‐channels blocking peptides from scorpions of the genus Centruroides

M. Corona, E. Wanke, E. Merino, 2002, FEBS letters.

Isolation of a Long-Lasting eag-Related Gene-Type K+ Current in MMQ Lactotrophs and Its Accommodating Role during Slow Firing and Prolactin Release

E. Redaelli, E. Wanke, O. Crociani, 2002, The Journal of Neuroscience.

Resurgent Current and Voltage Sensor Trapping Enhanced Activation by a β-Scorpion Toxin Solely in Nav1.6 Channel

F. Tempia, E. Wanke, T. Sacco, 2006, Journal of Biological Chemistry.

Identification of an Nav1.1 sodium channel (SCN1A) loss-of-function mutation associated with familial simple febrile seizures.

Aldo Quattrone, Massimo Mantegazza, Antonio Gambardella, 2005, Proceedings of the National Academy of Sciences of the United States of America.

Target Promiscuity and Heterogeneous Effects of Tarantula Venom Peptides Affecting Na+ and K+ Ion Channels*

E. Redaelli, E. Wanke, A. Arcangeli, 2009, The Journal of Biological Chemistry.

Identification of an Nav1.1 sodium channel (SCN1A) loss-of-function mutation associated with familial simple febrile seizures.

S. Franceschetti, E. Wanke, A. Quattrone, 2005, Proceedings of the National Academy of Sciences of the United States of America.