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Am J Physiol Cell Physiol
2016 Dec 01;3116:C942-C944. doi: 10.1152/ajpcell.00309.2016.
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H(OH), H(OH), H(OH): a holiday perspective. Focus on "Mouse Slc4a11 expressed in Xenopus oocytes is an ideally selective H+/OH- conductance pathway that is stimulated by rises in intracellular and extracellular pH".
Bonanno,
Molecular mechanisms underlying the corneal endothelial pump.
2012, Pubmed
Bonanno,
Molecular mechanisms underlying the corneal endothelial pump.
2012,
Pubmed
Gröger,
SLC4A11 prevents osmotic imbalance leading to corneal endothelial dystrophy, deafness, and polyuria.
2010,
Pubmed
Han,
Mice with a targeted disruption of Slc4a11 model the progressive corneal changes of congenital hereditary endothelial dystrophy.
2013,
Pubmed
Kao,
Multifunctional ion transport properties of human SLC4A11: comparison of the SLC4A11-B and SLC4A11-C variants.
2016,
Pubmed
Loganathan,
Functional assessment of SLC4A11, an integral membrane protein mutated in corneal dystrophies.
2016,
Pubmed
,
Xenbase
Myers,
Mouse Slc4a11 expressed in Xenopus oocytes is an ideally selective H+/OH- conductance pathway that is stimulated by rises in intracellular and extracellular pH.
2016,
Pubmed
,
Xenbase
Park,
NaBC1 is a ubiquitous electrogenic Na+ -coupled borate transporter essential for cellular boron homeostasis and cell growth and proliferation.
2004,
Pubmed
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Xenbase
Vilas,
Transmembrane water-flux through SLC4A11: a route defective in genetic corneal diseases.
2013,
Pubmed
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Xenbase
Vithana,
Mutations in sodium-borate cotransporter SLC4A11 cause recessive congenital hereditary endothelial dystrophy (CHED2).
2006,
Pubmed
