Evidence map›Paper›PMID 19372380›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

Hv1 proton channels are required for high-level NADPH oxidase-dependent superoxide production during the phagocyte respiratory burst.

I Scott Ramsey, Evelyne Ruchti, J Stefan Kaczmarek, David E Clapham

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers.

0numbers the graph read from it
0cells of the map it votes in
155citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

155 citing papers in PubMed, 257 citations in OpenAlex.

  1. Trial
  2. Review
  3. Voltage-gated proton channel Hv1/VSOP regulates reciprocal interactions between F-actin and endosomes in microglia.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Validation of HvFrontiers in cellular neuroscience · 2025
    Article
  9. Fluctuating hydrogen-bond network of the Hv1 ion channel.Computational and structural biotechnology journal · 2025
    Article
  10. Article
  11. Quantitative insights into the mechanism of proton conduction and selectivity for the human voltage-gated proton channel Hv1.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  12. Review
  13. Review
  14. Inhibition of the HFrontiers in immunology · 2024
    Article
  15. Review
  16. The vacuolar anti-Frontiers in immunology · 2024
    Article
  17. Trapping Charge Mechanism in Hv1 Channels (International journal of molecular sciences · 2023
    Article
  18. Article
  19. NaInternational journal of molecular sciences · 2023
    Review
  20. Review

95 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

4 authors at 1 institution in 1 country.

I Scott RamseyHoward Hughes Medical Institute, Department of Neurobiology, Harvard Medical School, and Department of Cardiovascular Research, Manton Center for Orphan Disease, Children's Hospital, 320 Longwood Avenue, Boston, MA 02115, USA.
Evelyne Ruchti
J Stefan Kaczmarek
David E Clapham
Howard Hughes Medical Institute · US

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI POMEROY, SCOTT LOREN · 1985 to 2015
$26.2M
RESEARCH METHODS IN PEDIATRICS HEART DISEASET32HL007572 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI Sarah D DE FERRANTI, Jane W. Newburger · 1985 to 2026
$13.0M
Howard Hughes Medical InstituteNHLBI NIH HHS T32 HL007572NICHD NIH HHS P30 HD018655NICHD NIH HHS P30-HD18655PHS HHS T32 HLO7572
6 · The paper itself

Abstract

Granulocytes generate a "respiratory burst" of NADPH oxidase-dependent superoxide anion (O(2)(-*)) production that is required for efficient clearance of bacterial pathogens. Hv1 mediates a voltage-gated H(+) channel activity that is proposed to serve a charge-balancing role in granulocytic phagocytes such as neutrophils and eosinophils. Using mice in which the gene encoding Hv1 is replaced by beta-Geo reporter protein sequence, we show that Hv1 expression is required for measurable voltage-gated H(+) current in unstimulated phagocytes. O(2)(-*) production is substantially reduced in the absence of Hv1, suggesting that Hv1 contributes a majority of the charge compensation required for optimal NADPH oxidase activity. Despite significant reduction in superoxide production, Hv1(-/-) mice are able to clear several types of bacterial infections.

Indexed as

Respiratory BurstAnimalsGranulocytesHL-60 CellsHumansIon ChannelsMiceMice, KnockoutNADPH OxidasesPhagocytesSuperoxidesHv1 proton channel, mouseIon ChannelsNADPH OxidasesSuperoxides

Identifiers

PMID19372380
PMCPMC2669790
OpenAlexW2063340476

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.