Results 31 to 40 of about 3,909 (203)

Expression of Pendrin Periostin in Allergic Rhinitis Chronic Rhinosinusitis

open access: yesAllergology International, 2012
Background: : Pendrin and periostin are newly identified mediators of the inflammatory process. The expression of these proteins in human sinonasal tissue and their roles in allergic rhinitis and chronic rhinosinusitis remain to be elucidated. This study
Akihiro Ishida   +7 more
doaj   +1 more source

Renal intercalated cells and blood pressure regulation

open access: yesKidney Research and Clinical Practice, 2017
Type B and non-A, non-B intercalated cells are found within the connecting tubule and the cortical collecting duct. Of these cell types, type B intercalated cells are known to mediate Cl⁻ absorption and HCO₃⁻ secretion largely through pendrin-dependent ...
Susan M. Wall
doaj   +1 more source

Novel roles for chloride channels, exchangers, and regulators in chronic inflammatory airway diseases [PDF]

open access: yes, 2015
Chloride transport proteins play critical roles in inflammatory airway diseases, contributing to the detrimental aspects of mucus overproduction, mucus secretion, and airway constriction.
Berry, Kayla N   +3 more
core   +4 more sources

Effect of Known Inhibitors of Ion Transport on Pendrin (SLC26A4) Activity in a Human Kidney Cell Line

open access: yesCellular Physiology and Biochemistry, 2016
Background/Aims: Pendrin is a Cl-/I-/HCO3- exchanger playing a fundamental role in controlling blood pressure and airway function, therefore representing an attractive target for the treatment of hypertensive states and respiratory distresses.
Emanuele Bernardinelli   +4 more
doaj   +1 more source

DNAJC14 Ameliorates Inner Ear Degeneration in the DFNB4 Mouse Model

open access: yesMolecular Therapy: Methods & Clinical Development, 2020
The His723Arg (H723R) mutation in SLC26A4, encoding pendrin, is the most prevalent mutation in East Asia, resulting in DFNB4, an autosomal recessive type of genetic hearing loss.
Hye Ji Choi   +10 more
doaj   +1 more source

Non-syndromic enlarged vestibular aqueduct caused by novel compound mutations of the SLC26A4 gene: a case report and literature review

open access: yesFrontiers in Genetics, 2023
Enlarged vestibular aqueduct is an autosomal genetic disease mainly caused by mutations in the SLC26A4 gene and includes non-syndromic and syndromic types.
Yunhua Huang   +13 more
doaj   +1 more source

Expression of Human Pendrin in Diseased Thyroids [PDF]

open access: yesJournal of Histochemistry & Cytochemistry, 2003
We examined pendrin expression in various diseased thyroid tissues by immunohistochemistry (IHC) using antiserum raised against human pendrin and by real-time quantitative RT-PCR. In normal thyroids the antiserum reacted with the apical membrane of follicular cells and its immunoreactivity was faint.
Tetsuo, Kondo   +6 more
openaire   +2 more sources

The Human Pendrin Promoter Contains two N4 GAS Motifs with Different Functional Relevance

open access: yesCellular Physiology and Biochemistry, 2013
Background: Pendrin, an anion exchanger associated with the inner ear, thyroid and kidney, plays a significant role in respiratory tissues and diseases, where its expression is increased following IL-4 and IL-13 exposure.
Simone Vanoni   +7 more
doaj   +1 more source

Atypical Presentation of Enlarged Vestibular Aqueducts Caused by SLC26A4 Variants

open access: yesChildren, 2022
Enlarged vestibular aqueduct is the most common inner ear malformation in pediatric patients with sensorineural hearing loss. Here, we report a new presentation of enlarged vestibular aqueduct in a Korean family.
Jun Chul Byun   +2 more
doaj   +1 more source

Functional Studies of Deafness-Associated Pendrin and Prestin Variants. [PDF]

open access: yesInt J Mol Sci
Pendrin and prestin are evolutionary-conserved membrane proteins that are essential for normal hearing. Dysfunction of these proteins results in hearing loss in humans, and numerous deafness-associated pendrin and prestin variants have been identified in patients. However, the pathogenic impacts of many of these variants are ambiguous.
Takahashi S   +3 more
europepmc   +4 more sources

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