Papers associated with right (and scn5a)

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	Distinct functional properties of two electrogenic isoforms of the SLC34 Na-Pi cotransporter., Mizutani N., Physiol Rep. July 1, 2019; 7 (14): e14156.
	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.
	Xenopus borealis as an alternative source of oocytes for biophysical and pharmacological studies of neuronal ion channels., Cristofori-Armstrong B., Sci Rep. January 12, 2015; 5 14763.
	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.
	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.
	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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