Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

SLC26A9-mediated chloride secretion prevents mucus obstruction in airway inflammation.

The Journal of clinical investigation - 1 Oct 2012

Anagnostopoulou Pinelopi, Riederer Brigitte, Duerr Julia, Michel Sven, Binia Aristea, Agrawal Raman, Liu Xuemei, Kalitzki Katrin, Xiao Fang, Chen Mingmin, Schatterny Jolanthe, Hartmann Dorothee, Thum Thomas, Kabesch Michael, Soleimani Manoocher, Seidler Ursula, Mall Marcus A

Abstract excerpt

Asthma is a chronic condition with unknown pathogenesis, and recent evidence suggests that enhanced airway epithelial chloride (Cl-) secretion plays a role in the disease. However, the molecular mechanism underlying Cl- secretion and its relevance in asthma pathophysiology remain unknown. To determine the role of the solute carrier family 26, member 9 (SLC26A9) Cl- channel in asthma, we induced Th2-mediated...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Airway Obstruction
Share to Antiporters

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Bronchitis

Share to Chlorides

Share to Interleukin-13

Share to Ion Transport

Share to Sulfate Transporters

Source

Open in PubMed Open full text

Identifiers

PMID: 22945630
DOI: 10.1172/JCI60429
PMCID: PMC3461899

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

SLC26A9-mediated chloride secretion prevents mucus obstruction in airway inflammation.PMID 22945630Read ↗

Allergic airway inflammation induces a pro-secretory epithelial ion transport phenotype in miceSemantic proximity Read ↗

Synergy in Cystic Fibrosis Therapies: Targeting SLC26A9.Semantic proximity Read ↗

A novel SLC26A9 inhibitor, S9-A13, reveals a minor contribution of SLC26A9 to constitutive airway chloride secretionSemantic proximity Read ↗

CDH26 amplifies airway epithelial IL-4 receptor α signaling in asthmaSemantic proximity Read ↗

Inhibition of the sodium-dependent HCO3- transporter SLC4A4, produces a cystic fibrosis-like airway disease phenotype.Semantic proximity Read ↗

Dynamic regulation of airway surface liquid pH by TMEM16A and SLC26A4 in cystic fibrosis nasal epithelia with rare mutations.Semantic proximity Read ↗

SLC26A9 stimulates CFTR expression and function in human bronchial cell linesSemantic proximity Read ↗

TMEM16A chloride channel does not drive mucus productionSemantic proximity Read ↗

IL-13 and Epidermal Growth Factor Receptor Have Critical but Distinct Roles in Epithelial Cell Mucin ProductionSemantic proximity Read ↗

Bicarbonate and functional CFTR channel are required for proper mucin secretion and link cystic fibrosis with its mucus phenotype.Semantic proximity Read ↗

IL-4 Receptor Signaling in Clara Cells Is Required for Allergen-Induced Mucus ProductionSemantic proximity Read ↗

Mucus Hyperconcentration as a Unifying Aspect of the Chronic Bronchitic PhenotypeSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.