Evidence map›Paper›PMID 24659781›Full record

ArticleThe Journal of biological chemistry2014

Tight junctional localization of claudin-16 is regulated by syntaxin 8 in renal tubular epithelial cells.

Akira Ikari, Chie Tonegawa, Ayumi Sanada, Toru Kimura, Hideki Sakai, Hisayoshi Hayashi, Hajime Hasegawa, Masahiko Yamaguchi, Yasuhiro Yamazaki, Satoshi Endo and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. The role of claudins in homeostasis.Nature reviews. Nephrology · 2023
    Review
  2. Human microsporidian pathogenJournal of cell science · 2021
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Developmental Expression of Claudins in the Mammary Gland.Journal of mammary gland biology and neoplasia · 2017
    Article
  11. Review
  12. Claudins and mineral metabolism.Current opinion in nephrology and hypertension · 2016
    Review
  13. Review
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

12 authors at 5 institutions in 1 country.

Akira IkariFrom the Laboratory of Biochemistry, Department of Biopharmaceutical Sciences, Gifu Pharmaceutical University, Gifu 501-1196, Japan.
Chie Tonegawa
Ayumi Sanada
Toru Kimura
Hideki Sakai
Hisayoshi Hayashi
Hajime Hasegawa
Masahiko Yamaguchi
Yasuhiro Yamazaki
Satoshi Endo
Toshiyuki Matsunaga
Junko Sugatani
University of Shizuoka · JPGifu Pharmaceutical University · JPKyorin University · JPSocial Insurance Saitama Chuo Hospital · JPUniversity of Toyama · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Claudin-16 (CLDN16) regulates the paracellular reabsorption of Mg(2+) in the thick ascending limb of Henle's loop. However, the mechanism regulating the tight junctional localization of CLDN16 remains unknown. In yeast two-hybrid systems, we found that CLDN16 bound to syntaxin 8 (STX8), a target soluble N-ethylmaleimide-sensitive factor attachment protein receptor. We have examined the effect of STX8 on the localization and function of CLDN16 using Madin-Darby canine kidney cells expressing FLAG-tagged CLDN16. A pulldown assay showed that the carboxyl cytoplasmic region of human CLDN16 bound to STX8. CLDN16 was localized in the thick ascending limb, whereas STX8 was widely distributed throughout the rat kidney. An association between CLDN16 and STX8 was observed in rat renal homogenates and Madin-Darby canine kidney cells. STX8 siRNA decreased the cell surface localization of CLDN16 and transepithelial electrical resistance and permeability to Mg(2+) but increased the co-localization of CLDN16 with early endosome and lysosome markers. Dephosphorylation of CLDN16 by protein kinase A inhibitors and S217A mutant, a dephosphorylated form, decreased the association with STX8 and the cell surface localization of CLDN16. Recycling assays indicated that STX8 siRNA decreased the trafficking of CLDN16 to the plasma membrane without affecting endocytosis. Dominant negative Rab11 and recycling inhibitor primaquine decreased the cell surface localization of CLDN16, which was similar to that in STX8 siRNA-transfected cells. These results suggest that STX8 mediates the recycling of CLDN16 and constitutes an important component of the CLDN16 trafficking machinery in the kidney.

Indexed as

Amino Acid SubstitutionAnimalsClaudinsCyclic AMP-Dependent Protein KinasesDogsEndosomesEpithelial CellsHumansKidney Tubules, ProximalLysosomesMadin Darby Canine Kidney CellsMaleMutation, MissensePhosphorylationProtein BindingProtein Transportclaudin 16ClaudinsCyclic AMP-Dependent Protein KinasesQa-SNARE ProteinsClaudinConfocal MicroscopyKidneyMagnesium HomeostasisSyntaxinTight JunctionsTrafficking

Identifiers

PMID24659781
PMCPMC4036323
OpenAlexW2043133537

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.