Recombinant Mouse Pendrin (Slc26a4), partial

1. The ablation of the Cl-/HCO3- exchanger Pendrin enhances the magnitude of salt wasting by hydrochlorothiazide (HCTZ). PMID: 28750403
2. Here, the authors show that the mouse endolymphatic sac absorbs fluid in an SLC26A4-dependent fashion. PMID: 28994389
3. Acute genetic ablation of pendrin lowers blood pressure. PMID: 28064162
4. Data, including data from studies using transgenic mice, suggest that over-expression of IL4 (interleukin 4) in thyroid tissue/cells up-regulates expression of Duox1 (dual oxidase 1), Duoxa1 (dual oxidase maturation factor 1), and Slc26a4 (pendrin) in thyroid tissue/cells; expression of Slc5a5 (sodium-iodide symporter) is down-regulated. PMID: 27599561
5. Study showed that early re-induction of Slc26a4 expression can prevent fluctuation of hearing in our Slc26a4-insufficient mouse model. Restoration of SLC26A4 expression and function could reduce or prevent fluctuation of hearing in enlargement of the vestibular aqueduct patients. PMID: 27155149
6. decreased plasma K(+) levels promote pendrin induction by aldosterone, which, in concert with Na(+)-Cl(-) cotransporter, counteracts the progression of hypokalemia but promotes hypertension in primary aldosterone excess. PMID: 28289181
7. The strial dysfunction and degeneration are the primary causes of irreversible progressive hearing loss in our Slc26a4-insufficient mouse model of vestibular aqueduct syndrome. PMID: 26363152
8. Pendrin is expressed in the adrenal medulla, where it blunts stress-induced catecholamine release. PMID: 26173457
9. Pendrin gene ablation reduced ENaC-mediated Na(+) absorption by reducing channel open probability as well as by reducing channel density through changes in subunit total protein abundance and subcellular distribution. PMID: 25972513
10. The result provides insight into the role of Na+ transport in the development and regulation of endolymphatic hydrops due to pendrin mutations. PMID: 24752462
11. Insufficient availability of thyroid hormone during inner ear development plays an important role in the mechanism underlying deafness as a result of SLC26A4 mutations. PMID: 24760582
12. The results indicated not only the p.H723R allele was non-pathogenic in mice, but also a single p.H723R allele was sufficient to maintain normal inner ear physiology in heterozygous compound mice. PMID: 23755160
13. Together these data suggest that pertussis toxin contributes to pertussis pathology through the upregulation of pendrin, which promotes conditions favoring inflammatory pathology. PMID: 25069981
14. Using a transgenic mouse line in which all Slc26a4 expression was under the control of doxycycline, showed that fluctuations of hearing result from fluctuations of endocochlear potential and stria vascularis dysfunction in Slc26a4-insufficient mouse ears PMID: 24561068
15. This review summarizes recent studies in mouse models that have been developed to delineate the role of pendrin in the physiology of hearing PMID: 24429822
16. The co-regulation of pendrin and AQP5 membrane expression under chronic K(+)-deficiency indicates that these two molecules could cooperate as an osmosensor to rapidly detect and respond to alterations in luminal fluid osmolality. PMID: 24429825
17. Pendrin is regulated by acidosis and chloride intake in renal collecting ducts. PMID: 23383138
18. The mineralocorticoid sensitivity of pendrin expression in kidney, heart, thyroid and lung. PMID: 23235354
19. It was concluded that NO acts through cAMP to reduce pendrin total protein abundance by enhancing cAMP degradation. PMID: 22811483
20. Deletion of the Cl-/HCO3- exchanger pendrin downregulates calcium-absorbing proteins in the kidney and causes calcium wasting. PMID: 21873623
21. presence of SLC26A4 in apical plasma membranes of maturation ameloblasts is consistent with a potential function as a pH regulator PMID: 22243245
22. Varying the temporal expression of Slc26a4 revealed that E16.5 to P2 was the critical interval in which pendrin was required for acquisition of normal hearing. PMID: 21965328
23. There was a significant difference in the vestibular performance between wild-type and Slc26a4(tm1Dontuh/tm1Dontuh) mice, especially those exhibiting circling behavior. PMID: 21811566
24. Stretching and luminal acidification may alter cell-to-cell communication and lead to the observed retarded development of stria vascularis, which may be an important step on the path to deafness in Slc26a4(-/-) mice. PMID: 21423764
25. Data show that failure of fluid absorption in the endolymphatic sac due to lack of Slc26a4 expression appears to initiate cochlear enlargement in mice, and possibly humans, lacking functional Slc26a4 expression. PMID: 21103348
26. The present study aimed to characterize the intrinsic properties of pendrin by monitoring changes in the intracellular pH induced by variations of transmembrane anion gradients. PMID: 21073444
27. Pendrin modulates ENaC abundance and function within the cortical collecting duct, at least in part by increasing luminal [HCO(3)(-)] and/or pH. PMID: 20966128
28. two mutations abolished complex glycosylation of pendrin and prevented its targeting to the plasma membrane. PMID: 20128824
29. calcium oxalate stone formation in the inner ear is a result of an Slc26a4 mutation PMID: 20442411
30. Slc26a4 (pendrin) deletion impairs the secretion of bicarbonate in vivo and reduces apical Cl(-)/HCO(3)(-) exchanger activity in cells of the kidney collecting duct. PMID: 20375274
31. its presence in both the apical plasma membrane and the apical intracellular vesicles of type B and non-A-non-B intercalated cells suggests that HCO secretion may be regulated by trafficking between the two membrane compartments PMID: 12217866
32. pendrin is not responsible for formate-dependent NaCl reabsorption in the proximal tubule. PMID: 12372770
33. pendrin is expressed in the mouse distal convoluted tubule, collecting duct, and connecting tubule along the apical plasma membrane of non-A-non-B intercalated cells and in subapical cytoplasmic vesicles of type B intercalated cells. PMID: 12388426
34. potential role of pendrin in bicarbonate secretion and regulation of acid-base transport in the cortical collecting duct. PMID: 12427135
35. Pendrin is upregulated with aldosterone analogues and is critical in the pathogenesis of mineralocorticoid-induced hypertension and metabolic alkalosis. PMID: 12925556
36. pendrin serves a key role in the functioning of the basal and/or intermediate cells of the stria vascularis to maintain the endocochlear potential, but not in the potassium secretory function of the marginal cells. PMID: 14690057
37. Pendrin in the endolymphatic duct and sac, and the utricle, saccule, and external sulcus. Also in the spiral ligament, Claudius cells, Deiter's cells, and the spiral ganglion of the cochlea. PMID: 15350275
38. We conclude that Slc26a4 is upregulated with NaCl restriction and is critical in the maintenance of acid-base balance and in the renal conservation of Cl- and water during NaCl restriction. PMID: 15477386
39. Pendrin participates in the regulation of renal chloride excretion and arterial pH during dietary chloride restriction. PMID: 16670435
40. Slc26a4 is expressed in areas of the endolymphatic compartment known to play a role in endolymph reabsorption and absence of this protein leads to a profound prenatal endolymphatic hydrops. PMID: 17120770
41. SLC26A4 regulates blood pressure and arterial pH, likely by participating in the renal regulation of net acid and Cl- excretion. PMID: 17120771
42. Slc26a4(-/-) mice exhibit reduced pH and utricular endolymphatic potential and increased [Ca(2+)]. PMID: 17200157
43. The reduced ENaC protein abundance and function observed in Slc26a4-null mice contribute to their lower blood pressure and reduced ability to conserve Na(+) during NaCl restriction. PMID: 17686956
44. Pendrin-positive cells gradually disappeared by apoptosis from the inner part of the medullary collecting duct two weeks after birth. PMID: 17855646
45. free radical stress provides a link between loss of pendrin and loss of Kcnj10 in Slc26a4(-/-) mice and possibly in human patients suffering from Pendred syndrome. PMID: 17959752
46. CAII deficiency results in a significant decrease in the gene and protein expression of bicarbonate transport proteins from Slc26 gene family - Slc26a4 (pendrin) and Slc26a7. PMID: 18209476
47. Pendrin-mediated bicarbonate ion secretion in the renal tubule and anion transport in the endolymph may be regulated transcriptionally by systemic pH and aldosterone. PMID: 18322141
48. pendrin regulates airway surface liquid thickness and may be an important contributor to asthma exacerbations induced by viral infections or allergens PMID: 18641360
49. pendrin expression is primarily correlated with urinary Cl(-) excretion but not blood Cl(-). PMID: 18971389
50. mutations in the inwardly rectifying K(+) channel gene KCNJ10 are associated with nonsyndromic hearing loss in carriers of SLC26A4 mutations with an EVA/PS phenotype. PMID: 19426954

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KEGG: mmu:23985

STRING: 10090.ENSMUSP00000001253

UniGene: Mm.100187