Evidence map›Paper›PMID 22956539›Full record

ArticleJournal of cell science2012

Intracellular chloride channel protein CLIC1 regulates macrophage function through modulation of phagosomal acidification.

Lele Jiang, Kanin Salao, Hui Li, Joanna M Rybicka, Robin M Yates, Xu Wei Luo, Xin Xin Shi, Tamara Kuffner, Vicky Wang-Wei Tsai, Yasmin Husaini and 6 more

Open access · greenAbstract read
In one paragraph

Article in Journal of cell science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

63 citing papers in PubMed, 92 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. CLIC1 Supports Mechanisms Related to Platelet Activation and Thrombosis.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Intracellular chloride channel 1 and tumor.American journal of cancer research · 2023
    Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

3 more citing papers are in PubMed but not listed here.

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

16 authors at 4 institutions in 2 countries.

Lele JiangSt Vincent's Centre for Applied Medical Research, St Vincent's Hospital and University of New South Wales, Sydney, NSW 2010, Australia. l.jiang@amr.org.au
Kanin Salao
Hui Li
Joanna M Rybicka
Robin M Yates
Xu Wei Luo
Xin Xin Shi
Tamara Kuffner
Vicky Wang-Wei Tsai
Yasmin Husaini
Liyun Wu
David A Brown
Thomas Grewal
Louise J Brown
Paul M G Curmi
Samuel N Breit
UNSW Sydney · AUUniversity of Calgary · CAMacquarie University · AUThe University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intracellular chloride channel protein 1 (CLIC1) is a 241 amino acid protein of the glutathione S transferase fold family with redox- and pH-dependent membrane association and chloride ion channel activity. Whilst CLIC proteins are evolutionarily conserved in Metazoa, indicating an important role, little is known about their biology. CLIC1 was first cloned on the basis of increased expression in activated macrophages. We therefore examined its subcellular localisation in murine peritoneal macrophages by immunofluorescence confocal microscopy. In resting cells, CLIC1 is observed in punctate cytoplasmic structures that do not colocalise with markers for endosomes or secretory vesicles. However, when these macrophages phagocytose serum-opsonised zymosan, CLIC1 translocates onto the phagosomal membrane. Macrophages from CLIC1(-/-) mice display a defect in phagosome acidification as determined by imaging live cells phagocytosing zymosan tagged with the pH-sensitive fluorophore Oregon Green. This altered phagosomal acidification was not accompanied by a detectable impairment in phagosomal-lysosomal fusion. However, consistent with a defect in acidification, CLIC1(-/-) macrophages also displayed impaired phagosomal proteolytic capacity and reduced reactive oxygen species production. Further, CLIC1(-/-) mice were protected from development of serum transfer induced K/BxN arthritis. These data all point to an important role for CLIC1 in regulating macrophage function through its ion channel activity and suggest it is a suitable target for the development of anti-inflammatory drugs.

Indexed as

AcidsAnimalsArthritisChloride ChannelsCytoskeletal ProteinsEzrinGlycolatesHydrogen-Ion ConcentrationIntracellular MembranesLysosomesMacrophages, PeritonealMembrane ProteinsMiceMicrofilament ProteinsNADPH OxidasesPhagosomesAcidsChloride ChannelsClic1 protein, mouseCytoskeletal ProteinsEzrinGlycolatesMembrane ProteinsMicrofilament ProteinsMK 473moesinNADPH OxidasesRAC2 GTP-Binding Proteinrac GTP-Binding ProteinsradixinReactive Oxygen SpeciesrhoA GTP-Binding Protein

Identifiers

PMID22956539
PMCPMC3561857
OpenAlexW2025700341

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.