Roope Männikkö
Affiliations: | 2000-2003 | Departmen of Neuroscience | Karolinska Institute, Stockholm, Sweden |
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| Salpietro V, Galassi-Deforie V, Efthymiou S, et al. (2022) De novo KCNA6 variants with attenuated K 1.6 channel deactivation in patients with epilepsy. Epilepsia |
| Carpenter JC, Männikkö R, Heffner C, et al. (2021) Progressive myoclonus epilepsy KCNC1 variant causes a developmental dendritopathy. Epilepsia. 62: 1256-1267 |
| Vivekanandam V, Männikkö R, Matthews E, et al. (2020) Improving genetic diagnostics of skeletal muscle channelopathies. Expert Review of Molecular Diagnostics. 20: 725-736 |
| Franklin JP, Cooper-Knock J, Baheerathan A, et al. (2020) Concurrent sodium channelopathies and amyotrophic lateral sclerosis supports shared pathogenesis. Amyotrophic Lateral Sclerosis & Frontotemporal Degeneration. 1-4 |
| Echaniz-Laguna A, Biancalana V, Nadaj-Pakleza A, et al. (2020) Homozygous C-terminal loss-of-function Na1.4 variant in a patient with congenital myasthenic syndrome. Journal of Neurology, Neurosurgery, and Psychiatry |
| Veronica Tan S, Suetterlin K, Männikkö R, et al. (2020) In vivo assessment of interictal sarcolemmal membrane properties in hypokalaemic and hyperkalaemic periodic paralysis. Clinical Neurophysiology : Official Journal of the International Federation of Clinical Neurophysiology. 131: 816-827 |
| Thor MG, Vivekanandam V, Sampedro-Castañeda M, et al. (2019) Myotonia in a patient with a mutation in an S4 arginine residue associated with hypokalaemic periodic paralysis and a concomitant synonymous CLCN1 mutation. Scientific Reports. 9: 17560 |
| Myshkin MY, Männikkö R, Krumkacheva OA, et al. (2019) Cell-Free Expression of Sodium Channel Domains for Pharmacology Studies. Noncanonical Spider Toxin Binding Site in the Second Voltage-Sensing Domain of Human Na1.4 Channel. Frontiers in Pharmacology. 10: 953 |
| Türkdoğan D, Matthews E, Usluer S, et al. (2019) Possible role of skeletal muscle mutation in apnea during seizure. Epilepsia Open. 4: 498-503 |
| Salpietro V, Dixon CL, Guo H, et al. (2019) AMPA receptor GluA2 subunit defects are a cause of neurodevelopmental disorders. Nature Communications. 10: 3094 |