| The solute carrier family 26 member 9 modifies rapidly progressing cystic fibrosis associated with homozygous F508del CFTR mutation. | The solute carrier family 26 member 9 modifies rapidly progressing cystic fibrosis associated with homozygous F508del CFTR mutation.
Luo S, Rollins S, Schmitz-Abe K, Tam A, Li Q, Shi J, Lin J, Wang R, Agrawal PB. | 08/2/2024 |
| The role of the STAS domain in SLC26A9 for chloride ion transporter function. | The role of the STAS domain in SLC26A9 for chloride ion transporter function.
Omori S, Hanazono Y, Nishi H, Kinoshita K., Free PMC Article | 07/9/2024 |
| Pathogenic Relationships in Cystic Fibrosis and Renal Diseases: CFTR, SLC26A9 and Anoctamins. | Pathogenic Relationships in Cystic Fibrosis and Renal Diseases: CFTR, SLC26A9 and Anoctamins.
Kunzelmann K, Ousingsawat J, Kraus A, Park JH, Marquardt T, Schreiber R, Buchholz B., Free PMC Article | 09/16/2023 |
| Identification of single nucleotide variants in SLC26A9 gene in patients with cystic fibrosis (p.Phe508del homozygous) and its association to Orkambi(R) (Lumacaftor and Ivacaftor) response in vitro. | Identification of single nucleotide variants in SLC26A9 gene in patients with cystic fibrosis (p.Phe508del homozygous) and its association to Orkambi® (Lumacaftor and Ivacaftor) response in vitro.
Santos LG, Pereira SV, Kmit AHP, Bonadia LC, Bertuzzo CS, Ribeiro JD, Mazzola TN, Marson FAL. | 05/22/2023 |
| SLC26A9 deficiency causes gastric intraepithelial neoplasia in mice and aggressive gastric cancer in humans. | SLC26A9 deficiency causes gastric intraepithelial neoplasia in mice and aggressive gastric cancer in humans.
Liu X, Li T, Ma Z, Riederer B, Yuan D, Zhu J, Li Y, An J, Wen G, Jin H, Yang X, Seidler U, Tuo B., Free PMC Article | 06/18/2022 |
| Expression of SLC26A9 in Airways and Its Potential Role in Asthma. | Expression of SLC26A9 in Airways and Its Potential Role in Asthma.
Ousingsawat J, Centeio R, Schreiber R, Kunzelmann K., Free PMC Article | 04/16/2022 |
| SLC26A9 SNP rs7512462 is not associated with lung disease severity or lung function response to ivacaftor in cystic fibrosis patients with G551D-CFTR. | SLC26A9 SNP rs7512462 is not associated with lung disease severity or lung function response to ivacaftor in cystic fibrosis patients with G551D-CFTR.
Eastman AC, Pace RG, Dang H, Aksit MA, Vecchio-Pagán B, Lam AN, O'Neal WK, Blackman SM, Knowles MR, Cutting GR., Free PMC Article | 02/12/2022 |
| SLC26A9 is selected for endoplasmic reticulum associated degradation (ERAD) via Hsp70-dependent targeting of the soluble STAS domain. | SLC26A9 is selected for endoplasmic reticulum associated degradation (ERAD) via Hsp70-dependent targeting of the soluble STAS domain.
Needham PG, Goeckeler-Fried JL, Zhang C, Sun Z, Wetzel AR, Bertrand CA, Brodsky JL., Free PMC Article | 01/29/2022 |
| Alterations in SLC4A2, SLC26A7 and SLC26A9 Drive Acid-Base Imbalance in Gastric Neuroendocrine Tumors and Uncover a Novel Mechanism for a Co-Occurring Polyautoimmune Scenario. | Alterations in SLC4A2, SLC26A7 and SLC26A9 Drive Acid-Base Imbalance in Gastric Neuroendocrine Tumors and Uncover a Novel Mechanism for a Co-Occurring Polyautoimmune Scenario.
Calvete O, Reyes J, Valdés-Socin H, Martin P, Marazuela M, Barroso A, Escalada J, Castells A, Torres-Ruiz R, Rodríguez-Perales S, Currás-Freixes M, Benítez J., Free PMC Article | 01/8/2022 |
| Synergy in Cystic Fibrosis Therapies: Targeting SLC26A9. | Synergy in Cystic Fibrosis Therapies: Targeting SLC26A9.
Pinto MC, Quaresma MC, Silva IAL, Railean V, Ramalho SS, Amaral MD., Free PMC Article | 01/8/2022 |
| findings indicate that an increase in SLC26A9 expression in ductal cells of the pancreas delays the age at onset of diabetes, suggesting a CFTR-agnostic treatment for a major complication of CF. | Increased expression of anion transporter SLC26A9 delays diabetes onset in cystic fibrosis.
Lam AN, Aksit MA, Vecchio-Pagan B, Shelton CA, Osorio DL, Anzmann AF, Goff LA, Whitcomb DC, Blackman SM, Cutting GR., Free PMC Article | 07/25/2020 |
| The anion-conducting transporter solute carrier family 26 member 9 (SLC26A9) localizes to the tight junction in well-differentiated bronchi epithelial cell from non-cystic fibrosis (CF) patients, suggesting that F508del-CF transmembrane conductance regulator (CFTR) enhances proteasomal SLC26A9 degradation. | The anion transporter SLC26A9 localizes to tight junctions and is degraded by the proteasome when co-expressed with F508del-CFTR.
Sato Y, Thomas DY, Hanrahan JW., Free PMC Article | 06/27/2020 |
| Treatment response to ivacaftor, which aims to improve CFTR-channel opening probability in cystic fibrosis patients with gating mutations, shows substantial variability in response, 28% of which can be explained by rs7512462 in SLC26A9. | Cystic fibrosis gene modifier SLC26A9 modulates airway response to CFTR-directed therapeutics.
Strug LJ, Gonska T, He G, Keenan K, Ip W, Boëlle PY, Lin F, Panjwani N, Gong J, Li W, Soave D, Xiao B, Tullis E, Rabin H, Parkins MD, Price A, Zuberbuhler PC, Corvol H, Ratjen F, Sun L, Bear CE, Rommens JM., Free PMC Article | 03/3/2018 |
| when SLC26A9 is coexpressed with F508del CFTR, its trafficking defect leads to a PDZ motif-sensitive intracellular retention of SLC26A9. | The CFTR trafficking mutation F508del inhibits the constitutive activity of SLC26A9.
Bertrand CA, Mitra S, Mishra SK, Wang X, Zhao Y, Pilewski JM, Madden DR, Frizzell RA., Free PMC Article | 08/5/2017 |
| SLC26A9 single nucleotide polymorphisms modify prenatal exocrine pancreatic damage in cystic fibrosis | Variants in Solute Carrier SLC26A9 Modify Prenatal Exocrine Pancreatic Damage in Cystic Fibrosis.
Miller MR, Soave D, Li W, Gong J, Pace RG, Boëlle PY, Cutting GR, Drumm ML, Knowles MR, Sun L, Rommens JM, Accurso F, Durie PR, Corvol H, Levy H, Sontag MK, Strug LJ., Free PMC Article | 07/4/2015 |
| We have identified two SLC26A9 mutations decreasing Cl- channel transport in patients with a CF-like lung disease. | Characterization of SLC26A9 in patients with CF-like lung disease.
Bakouh N, Bienvenu T, Thomas A, Ehrenfeld J, Liote H, Roussel D, Duquesnoy P, Farman N, Viel M, Cherif-Zahar B, Amselem S, Taam RA, Edelman A, Planelles G, Sermet-Gaudelus I. | 07/26/2014 |
| SLC26A9 is an epithelial chloride/bicarbonate channel that can interact with the CF transmembrane regulator (CFTR), the protein mutated in CF | Genetic modifiers of cystic fibrosis-related diabetes.
Blackman SM, Commander CW, Watson C, Arcara KM, Strug LJ, Stonebraker JR, Wright FA, Rommens JM, Sun L, Pace RG, Norris SA, Durie PR, Drumm ML, Knowles MR, Cutting GR., Free PMC Article | 12/14/2013 |
| Several SNPs in the 3' UTR of SLC26A9 (rs12031234, rs2282429, rs2282430)were associated with asthma in children with asthma. | SLC26A9-mediated chloride secretion prevents mucus obstruction in airway inflammation.
Anagnostopoulou P, Riederer B, Duerr J, Michel S, Binia A, Agrawal R, Liu X, Kalitzki K, Xiao F, Chen M, Schatterny J, Hartmann D, Thum T, Kabesch M, Soleimani M, Seidler U, Mall MA., Free PMC Article | 02/2/2013 |
| SLC26A9 polymorphisms lead to several function modifications (increased activity, decreased activity, altered protein expression), which could lead to a spectrum of pathophysiologies. | Functional analysis of nonsynonymous single nucleotide polymorphisms in human SLC26A9.
Chen AP, Chang MH, Romero MF., Free PMC Article | 12/8/2012 |
| Single nucleotide polymorphism in SLC26A9 gene is associated with cystic fibrosis. | Multiple apical plasma membrane constituents are associated with susceptibility to meconium ileus in individuals with cystic fibrosis.
Sun L, Rommens JM, Corvol H, Li W, Li X, Chiang TA, Lin F, Dorfman R, Busson PF, Parekh RV, Zelenika D, Blackman SM, Corey M, Doshi VK, Henderson L, Naughton KM, O'Neal WK, Pace RG, Stonebraker JR, Wood SD, Wright FA, Zielenski J, Clement A, Drumm ML, Boëlle PY, Cutting GR, Knowles MR, Durie PR, Strug LJ., Free PMC Article | 07/7/2012 |
| Report functional interaction between CFTR and SLC26A9 in polarized airway epithelial cells and in non-polarized HEK293 cells. | Differential contribution of SLC26A9 to Cl(-) conductance in polarized and non-polarized epithelial cells.
Ousingsawat J, Schreiber R, Kunzelmann K. | 04/21/2012 |
| the L683P mutation of SLC26A9 was found to reduce Cl(-) transport through SLC26A9 as well as the positive interaction exerted by SLC26A9 on CFTR ion transport activity | Characterization of the L683P mutation of SLC26A9 in Xenopus oocytes.
Avella M, Borgese F, Ehrenfeld J. | 08/27/2011 |
| The interactions between SLC26A9 and CFTR were studied, and an alternative hypothesis to their known interactions is presented. | SLC26A9 stimulates CFTR expression and function in human bronchial cell lines.
Avella M, Loriol C, Boulukos K, Borgese F, Ehrenfeld J. | 12/11/2010 |
| Observational study of gene-disease association. (HuGE Navigator) | Large-scale candidate gene analysis of spontaneous clearance of hepatitis C virus.
Mosbruger TL, Duggal P, Goedert JJ, Kirk GD, Hoots WK, Tobler LH, Busch M, Peters MG, Rosen HR, Thomas DL, Thio CL., Free PMC Article | 04/7/2010 |
| Functions as an anion conductance in the apical membranes of bronchial epithelium; contributes to transepithelial chloride currents under basal and cyclic AMP/protein kinase A-stimulated conditions. | SLC26A9 is a constitutively active, CFTR-regulated anion conductance in human bronchial epithelia.
Bertrand CA, Zhang R, Pilewski JM, Frizzell RA., Free PMC Article | 02/15/2010 |