Defective processing and expression of thiazide-sensitive Na-Cl cotransporter as a cause of Gitelman’s syndrome
Kunchaparty S, Palcso M, Berkman J, Velázquez H, Desir G, Bernstein P, Reilly R, Ellison D. Defective processing and expression of thiazide-sensitive Na-Cl cotransporter as a cause of Gitelman’s syndrome. American Journal Of Physiology 1999, 277: f643-f649. PMID: 10516289, DOI: 10.1152/ajprenal.1999.277.4.f643.Peer-Reviewed Original ResearchConceptsWild-type cloneTransport proteinsWild-type proteinWild-type geneUnglycosylated proteinProtein processingNa-Cl cotransporterUnglycosylated formEndoplasmic reticulumMutant clonesFunctional expressionDisease mutationsDefective processingXenopus oocytesProteinClonesThiazide-sensitive Na-Cl cotransporterSodium uptakeMutationsOocytesMembrane stainingAutosomal recessive disorderWestern blotThe T0 Domain of Rabbit KV1.3 Regulates Steady State Channel Protein Level
Segal A, Yao X, Desir G. The T0 Domain of Rabbit KV1.3 Regulates Steady State Channel Protein Level. Biochemical And Biophysical Research Communications 1999, 254: 54-64. PMID: 9920732, DOI: 10.1006/bbrc.1998.9801.Peer-Reviewed Original ResearchConceptsN-terminal regulatory regionVoltage-gated potassium channelsWild-type channelsRegulatory regionsPlasma membraneAmino terminusChannel assemblyChannel proteinsRecognition domainSingle-channel conductanceKv channelsChannel protein levelsProtein levelsProtein densityPotassium channelsOpen probabilityType channelsChannel conductanceKv1.3Fast inactivationDomainMembraneTerminusProteinInactivation