TUBULOPATHY

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Defective claudin-10 causes a novel variation of HELIX syndrome through compromised tight junction strand assembly
《Genes & Diseases》2022年第5期1301-1314,共14页Sebastian Sewerin Jorg Piontek Ria Schonauer Sonja Grunewald Angelika Rauch Steffen Neuber Carsten Bergmann Dorothee Gunzel Jan Halbritte 
supported by Deutsche Forschungsgemeinschaft(DFG)grants(No.GU 447/14-1,14-2 to DG,PI 837/4-1,4-2 to JP,and(No.HA 6908/2-1 to JH,respectively);by Else Kroner-Fresenius-Stiftung grant(No.2016_A52 to JH);JH receives additional funding from the DFG(No.6908/3-1);CB is an employee of Limbach and holds a part-time faculty appointment at the University of Freiburg;His research laboratory receives support from the DFG(No.BE 3910/8-1 and BE 3910/9-1);from the Federal Ministry of Education and Research(BMBF,No.01GM1903I and 01GM1903G).
Formation of claudin-10 based tight junctions(TJs)is paramount to paracellular Na+transport in multiple epithelia.Sequence variants in CLDN10 have been linked to HELIX syndrome,a salt-losing tubulopathy with altered h...
关键词：Claudin-10 HELIX syndrome Paracellular transport Salt-losing tubulopathy Tight junction 
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