Evidence map›Paper›PMID 19617429›Full record

ArticleThe Journal of experimental biology2009

CFTR Cl- channel functional regulation by phosphorylation of focal adhesion kinase at tyrosine 407 in osmosensitive ion transporting mitochondria rich cells of euryhaline killifish.

William S Marshall, Kaitlyn D Watters, Leah R Hovdestad, Regina R F Cozzi, Fumi Katoh

Open access · greenAbstract read
In one paragraph

Article in The Journal of experimental biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.5field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Regulation of the cystic fibrosis transmembrane conductance regulator anion channel by tyrosine phosphorylation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Osmoregulatory response to low salinities in the European sea bass embryos: a multi-site approach.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2013
    Article
  16. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

William S MarshallDepartment of Biology, St Francis Xavier University, PO Box 5000 Antigonish, Nova Scotia, Canada B2G 2W5. bmarshal@stfx.ca
Kaitlyn D Watters
Leah R Hovdestad
Regina R F Cozzi
Fumi Katoh
St. Francis Xavier University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cystic fibrosis transmembrane conductance regulator (CFTR) anion channels are the regulated exit pathway in Cl(-) secretion by teleost mitochondria rich salt secreting (MR) cells of the gill and opercular epithelia of euryhaline teleosts. By confocal light immunocytochemistry, immunogold transmission electron microscopy (TEM), and co-immunoprecipitation, using regular and phospho-antibodies directed against conserved sites, we found that killifish CFTR (kfCFTR) and the tyrosine kinase focal adhesion kinase (FAK) phosphorylated at Y407 (FAK pY407) are colocalized in the apical membrane and in subjacent membrane vesicles of MR cells. We showed previously that basolateral FAK pY407, unlike other FAK phosphorylation sites, is osmosensitive and dephosphorylates during hypotonic shock of epithelial cells (Marshall et al., 2008). In the present study, we found that hypotonic shock and the alpha(2)-adrenergic agonist clonidine (neither of which affects cAMP levels) rapidly and reversibly inhibit Cl(-) secretion by isolated opercular membranes, simultaneous with dephosphorylation of FAK pY407, located in the apical membrane. FAK pY407 is rephosphorylated and Cl(-) secretion rapidly restored by hypertonic shock as well as by forskolin and isoproterenol, which operate via cAMP and protein kinase A. We conclude that hormone mediated, cAMP dependent and osmotically mediated, cAMP independent pathways converge on a mechanism to activate CFTR and Cl(-) secretion, possibly through tyrosine phosphorylation of CFTR by FAK.

Indexed as

AnimalsClonidineColforsinCystic Fibrosis Transmembrane Conductance RegulatorElectrophysiologyFocal Adhesion Protein-Tyrosine KinasesFundulidaeHypertonic SolutionsHypotonic SolutionsIon TransportIsoproterenolMicroscopy, Electron, TransmissionMicroscopy, ImmunoelectronMitochondriaPhosphorylationProtein TransportClonidineColforsinCystic Fibrosis Transmembrane Conductance RegulatorFocal Adhesion Protein-Tyrosine KinasesHypertonic SolutionsHypotonic SolutionsIsoproterenolSympatholyticsSympathomimeticsTyrosine

Identifiers

PMID19617429
PMCPMC2712415
OpenAlexW2009122273

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.