Evidence map›Paper›PMID 19419761›Full record

ReviewCell calcium2009

Regulation of voltage-gated Ca2+ channels by lipids.

Mandy L Roberts-Crowley, Tora Mitra-Ganguli, Liwang Liu, Ann R Rittenhouse

Abstract readReview
In one paragraph

Review in Cell calcium, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Article
  3. BK channels mediate a presynaptic form of mGluR-LTD in the neonatal hippocampus.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Article
  5. Neutrophil diversity and function in health and disease.Signal transduction and targeted therapy · 2024
    Review
  6. Article
  7. Article
  8. Loss of ACOT7 potentiates seizures and metabolic dysfunction.American journal of physiology. Endocrinology and metabolism · 2019
    Article
  9. A Closely Associated Phospholipase C Regulates Cation Channel Function through Phosphoinositide Hydrolysis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Mandy L Roberts-CrowleyUniversity of Massachusetts Medical School, Worcester, MA 01655, USA.
Tora Mitra-Ganguli
Liwang Liu
Ann R Rittenhouse
University of Massachusetts Chan Medical School · US

Funding

Plasticity N-Type Ca2+ Channels in Sympathetic NeuronsR01NS034195 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI RITTENHOUSE, ANN R. · 2001 to 2005
$1.5M
TRAINING GRANT IN CELLULAR AND MOLECULAR NEUROBIOLOGYT32NS007366 · NINDS · WORCESTER FOUNDATION FOR BIOMEDICAL RES · PI REPPERT, STEVEN M. · 1995 to 2004
$628k
Role of Arachidonic Isoforms in Nerve Cell FunctionR21NS057473 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI RITTENHOUSE, ANN R. · 2007 to 2008
$391k
CA2+ CHANNELS IN SYMPATHETIC NEURONSR29NS034195 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI RITTENHOUSE, ANN R. · 1995 to 1999
–
NINDS NIH HHS NS057473NINDS NIH HHS NS07366NINDS NIH HHS NS34195NINDS NIH HHS R01 NS034195NINDS NIH HHS R21 NS057473NINDS NIH HHS R29 NS034195NINDS NIH HHS T32 NS007366
6 · The paper itself

Abstract

Great skepticism has surrounded the question of whether modulation of voltage-gated Ca(2+) channels (VGCCs) by the polyunsaturated free fatty acid arachidonic acid (AA) has any physiological basis. Here we synthesize findings from studies of both native and recombinant channels where micromolar concentrations of AA consistently inhibit both native and recombinant activity by stabilizing VGCCs in one or more closed states. Structural requirements for these inhibitory actions include a chain length of at least 18 carbons and multiple double bonds located near the fatty acid's carboxy terminus. Acting at a second site, AA increases the rate of VGCC activation kinetics, and in Ca(V)2.2 channels, increases current amplitude. We present evidence that phosphatidylinositol 4,5-bisphosphate (PIP(2)), a palmitoylated accessory subunit (beta(2a)) of VGCCs and AA appear to have overlapping sites of action giving rise to complex channel behavior. Their actions converge in a physiologically relevant manner during muscarinic modulation of VGCCs. We speculate that M(1) muscarinic receptors may stimulate multiple lipases to break down the PIP(2) associated with VGCCs and leave PIP(2)'s freed fatty acid tails bound to the channels to confer modulation. This unexpectedly simple scheme gives rise to unanticipated predictions and redirects thinking about lipid regulation of VGCCs.

Indexed as

Arachidonic AcidCalciumCalcium ChannelsGTP-Binding Protein alpha Subunits, Gq-G11LipidsPhosphatidylinositol 4,5-DiphosphatePhospholipases A2, CytosolicReceptors, MuscarinicArachidonic AcidCalciumCalcium ChannelsGTP-Binding Protein alpha Subunits, Gq-G11LipidsPhosphatidylinositol 4,5-DiphosphatePhospholipases A2, CytosolicReceptors, Muscarinic

Identifiers

PMID19419761
PMCPMC2964877
OpenAlexW2018111790

What OpenQuestion holds

Textmetadata
LicenceTDM
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.