Papers associated with brain (and scn5a)

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	Metamorphic gene regulation programs in Xenopus tropicalis tadpole brain., Raj S., PLoS One. January 1, 2023; 18 (6): e0287858.
	Electrophysiological characterization of a large set of novel variants in the SCN5A-gene: identification of novel LQTS3 and BrS mutations., Ortiz-Bonnin B., Pflugers Arch. August 1, 2016; 468 (8): 1375-87.
	Gain-of-function mutation in TASK-4 channels and severe cardiac conduction disorder., Friedrich C., EMBO Mol Med. July 1, 2014; 6 (7): 937-51.
	Molecular mechanism of allosteric modification of voltage-dependent sodium channels by local anesthetics., Arcisio-Miranda M., J Gen Physiol. November 1, 2010; 136 (5): 541-54.
	Induction of vertebrate regeneration by a transient sodium current., Tseng AS., J Neurosci. September 29, 2010; 30 (39): 13192-200.
	Pharmacological modulation of brain Nav1.2 and cardiac Nav1.5 subtypes by the local anesthetic ropivacaine., Cheng HW., Neurosci Bull. August 1, 2010; 26 (4): 289-96.
	Correlations between clinical and physiological consequences of the novel mutation R878C in a highly conserved pore residue in the cardiac Na+ channel., Zhang Y., Acta Physiol (Oxf). December 1, 2008; 194 (4): 311-23.
	GLUT8 is dispensable for embryonic development but influences hippocampal neurogenesis and heart function., Membrez M., Mol Cell Biol. June 1, 2006; 26 (11): 4268-76.
	A cardiac sodium channel mutation identified in Brugada syndrome associated with atrial standstill., Takehara N., J Intern Med. January 1, 2004; 255 (1): 137-42.
	Novel mutations in domain I of SCN5A cause Brugada syndrome., Vatta M., Mol Genet Metab. April 1, 2002; 75 (4): 317-24.
	Genetic and biophysical basis of sudden unexplained nocturnal death syndrome (SUNDS), a disease allelic to Brugada syndrome., Vatta M., Hum Mol Genet. February 1, 2002; 11 (3): 337-45.
	Functional suppression of sodium channels by beta(1)-subunits as a molecular mechanism of idiopathic ventricular fibrillation., Wan X., J Mol Cell Cardiol. October 1, 2000; 32 (10): 1873-84.
	SCN5A mutation (T1620M) causing Brugada syndrome exhibits different phenotypes when expressed in Xenopus oocytes and mammalian cells., Baroudi G., FEBS Lett. February 4, 2000; 467 (1): 12-6.
	Human SCN5A gene mutations alter cardiac sodium channel kinetics and are associated with the Brugada syndrome., Rook MB., Cardiovasc Res. December 1, 1999; 44 (3): 507-17.
	A single Na(+) channel mutation causing both long-QT and Brugada syndromes., Bezzina C., Circ Res. December 1, 1999; 85 (12): 1206-13.

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