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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
,
Xenbase Vilas,
Transmembrane water-flux through SLC4A11: a route defective in genetic corneal diseases.
2013,
Pubmed
,
Xenbase Vithana,
Mutations in sodium-borate cotransporter SLC4A11 cause recessive congenital hereditary endothelial dystrophy (CHED2).
2006,
Pubmed
