These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
256 related articles for article (PubMed ID: 23813972)
1. Transmembrane water-flux through SLC4A11: a route defective in genetic corneal diseases. Vilas GL; Loganathan SK; Liu J; Riau AK; Young JD; Mehta JS; Vithana EN; Casey JR Hum Mol Genet; 2013 Nov; 22(22):4579-90. PubMed ID: 23813972 [TBL] [Abstract][Full Text] [Related]
2. Functional assessment of SLC4A11, an integral membrane protein mutated in corneal dystrophies. Loganathan SK; Schneider HP; Morgan PE; Deitmer JW; Casey JR Am J Physiol Cell Physiol; 2016 Nov; 311(5):C735-C748. PubMed ID: 27558157 [TBL] [Abstract][Full Text] [Related]
4. Energy Shortage in Human and Mouse Models of SLC4A11-Associated Corneal Endothelial Dystrophies. Zhang W; Frausto R; Chung DD; Griffis CG; Kao L; Chen A; Azimov R; Sampath AP; Kurtz I; Aldave AJ Invest Ophthalmol Vis Sci; 2020 Jul; 61(8):39. PubMed ID: 32721020 [TBL] [Abstract][Full Text] [Related]
5. Fuchs Endothelial Corneal Dystrophy in a Heterozygous Carrier of Congenital Hereditary Endothelial Dystrophy Type 2 with a Novel Mutation in SLC4A11. Kim JH; Ko JM; Tchah H Ophthalmic Genet; 2015; 36(3):284-6. PubMed ID: 24502824 [TBL] [Abstract][Full Text] [Related]
6. High Throughput Assay Identifies Glafenine as a Corrector for the Folding Defect in Corneal Dystrophy-Causing Mutants of SLC4A11. Chiu AM; Mandziuk JJ; Loganathan SK; Alka K; Casey JR Invest Ophthalmol Vis Sci; 2015 Dec; 56(13):7739-53. PubMed ID: 26641551 [TBL] [Abstract][Full Text] [Related]
7. pH dependence of the Slc4a11-mediated H Quade BN; Marshall A; Parker MD Am J Physiol Cell Physiol; 2020 Aug; 319(2):C359-C370. PubMed ID: 32520610 [TBL] [Abstract][Full Text] [Related]
8. Mouse Slc4a11 expressed in Xenopus oocytes is an ideally selective H+/OH- conductance pathway that is stimulated by rises in intracellular and extracellular pH. Myers EJ; Marshall A; Jennings ML; Parker MD Am J Physiol Cell Physiol; 2016 Dec; 311(6):C945-C959. PubMed ID: 27681179 [TBL] [Abstract][Full Text] [Related]
9. Glutaminolysis is Essential for Energy Production and Ion Transport in Human Corneal Endothelium. Zhang W; Li H; Ogando DG; Li S; Feng M; Price FW; Tennessen JM; Bonanno JA EBioMedicine; 2017 Feb; 16():292-301. PubMed ID: 28117276 [TBL] [Abstract][Full Text] [Related]
10. Defective cell adhesion function of solute transporter, SLC4A11, in endothelial corneal dystrophies. Malhotra D; Jung M; Fecher-Trost C; Lovatt M; Peh GSL; Noskov S; Mehta JS; Zimmermann R; Casey JR Hum Mol Genet; 2020 Jan; 29(1):97-116. PubMed ID: 31691803 [TBL] [Abstract][Full Text] [Related]
11. Multifunctional ion transport properties of human SLC4A11: comparison of the SLC4A11-B and SLC4A11-C variants. Kao L; Azimov R; Shao XM; Frausto RF; Abuladze N; Newman D; Aldave AJ; Kurtz I Am J Physiol Cell Physiol; 2016 Nov; 311(5):C820-C830. PubMed ID: 27581649 [TBL] [Abstract][Full Text] [Related]
12. Molecular phenotype of SLC4A11 missense mutants: Setting the stage for personalized medicine in corneal dystrophies. Alka K; Casey JR Hum Mutat; 2018 May; 39(5):676-690. PubMed ID: 29327391 [TBL] [Abstract][Full Text] [Related]
13. Ophthalmic Nonsteroidal Anti-Inflammatory Drugs as a Therapy for Corneal Dystrophies Caused by SLC4A11 Mutation. Alka K; Casey JR Invest Ophthalmol Vis Sci; 2018 Aug; 59(10):4258-4267. PubMed ID: 30140924 [TBL] [Abstract][Full Text] [Related]
14. Human SLC4A11-C functions as a DIDS-stimulatable H⁺(OH⁻) permeation pathway: partial correction of R109H mutant transport. Kao L; Azimov R; Abuladze N; Newman D; Kurtz I Am J Physiol Cell Physiol; 2015 Jan; 308(2):C176-88. PubMed ID: 25394471 [TBL] [Abstract][Full Text] [Related]
15. Conditionally Immortal Slc4a11-/- Mouse Corneal Endothelial Cell Line Recapitulates Disrupted Glutaminolysis Seen in Slc4a11-/- Mouse Model. Zhang W; Ogando DG; Kim ET; Choi MJ; Li H; Tenessen JM; Bonanno JA Invest Ophthalmol Vis Sci; 2017 Jul; 58(9):3723-3731. PubMed ID: 28738416 [TBL] [Abstract][Full Text] [Related]
16. R125H, W240S, C386R, and V507I SLC4A11 mutations associated with corneal endothelial dystrophy affect the transporter function but not trafficking in PS120 cells. Li S; Hundal KS; Chen X; Choi M; Ogando DG; Obukhov AG; Bonanno JA Exp Eye Res; 2019 Mar; 180():86-91. PubMed ID: 30557570 [TBL] [Abstract][Full Text] [Related]
17. Congenital hereditary endothelial dystrophy caused by SLC4A11 mutations progresses to Harboyan syndrome. Siddiqui S; Zenteno JC; Rice A; Chacón-Camacho O; Naylor SG; Rivera-de la Parra D; Spokes DM; James N; Toomes C; Inglehearn CF; Ali M Cornea; 2014 Mar; 33(3):247-51. PubMed ID: 24351571 [TBL] [Abstract][Full Text] [Related]
18. SLC4A11 and the Pathophysiology of Congenital Hereditary Endothelial Dystrophy. Patel SP; Parker MD Biomed Res Int; 2015; 2015():475392. PubMed ID: 26451371 [TBL] [Abstract][Full Text] [Related]
20. IPSC-Derived Corneal Endothelial-like Cells Act as an Appropriate Model System to Assess the Impact of SLC4A11 Variants on Pre-mRNA Splicing. Brejchova K; Dudakova L; Skalicka P; Dobrovolny R; Masek P; Putzova M; Moosajee M; Tuft SJ; Davidson AE; Liskova P Invest Ophthalmol Vis Sci; 2019 Jul; 60(8):3084-3090. PubMed ID: 31323090 [TBL] [Abstract][Full Text] [Related] [Next] [New Search]