Evidence map›Paper›PMID 24062580›Full record

ArticlePhilosophical transactions of the Royal Society of London. Series B, Biological sciences2013

Actin dynamics rapidly reset chemoattractant receptor sensitivity following adaptation in neutrophils.

Sheel N Dandekar, Jason S Park, Grace E Peng, James J Onuffer, Wendell A Lim, Orion D Weiner

Abstract read
In one paragraph

Article in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Neutrophil diversity and function in health and disease.Signal transduction and targeted therapy · 2024
    Review
  2. Article
  3. Hyperactive Rac stimulates cannibalism of living target cells and enhances CAR-M-mediated cancer cell killing.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  4. UsingFrontiers in cell and developmental biology · 2021
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Projecting cell polarity into the next decade.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2013
    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

6 authors.

Sheel N DandekarDepartment of Biophysics, Genentech Hall, University of California, , 600 16th Street, San Francisco, CA 94158, USA.
Jason S Park
Grace E Peng
James J Onuffer
Wendell A Lim
Orion D Weiner

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007618 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ANDERSON, MARK S · 1985 to 2020
$29.6M
Cellular Control:Synthetic Signaling/Motility (RMI)PN2EY016546 · NEI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LIM, WENDELL A · 2005 to 2014
$16.0M
Integrative Program in Complex Biological System (ipCBS)T32EB009383 · NIBIB · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MARSHALL, WALLACE, WEINER, ORION D · 2009 to 2022
$3.2M
Signal Integration in Neutrophil ChemotaxisR01GM084040 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WEINER, ORION D · 2008 to 2015
$2.6M
NEI NIH HHS PN2EY016546NIBIB NIH HHS 5T32EB009383-03NIGMS NIH HHS R01 GM084040NIGMS NIH HHS T32 GM007618PHS HHS TG2-01153
6 · The paper itself

Abstract

Neutrophils are cells of the innate immune system that hunt and kill pathogens using directed migration. This process, known as chemotaxis, requires the regulation of actin polymerization downstream of chemoattractant receptors. Reciprocal interactions between actin and intracellular signals are thought to underlie many of the sophisticated signal processing capabilities of the chemotactic cascade including adaptation, amplification and long-range inhibition. However, with existing tools, it has been difficult to discern actin's role in these processes. Most studies investigating the role of the actin cytoskeleton have primarily relied on actin-depolymerizing agents, which not only block new actin polymerization but also destroy the existing cytoskeleton. We recently developed a combination of pharmacological inhibitors that stabilizes the existing actin cytoskeleton by inhibiting actin polymerization, depolymerization and myosin-based rearrangements; we refer to these processes collectively as actin dynamics. Here, we investigated how actin dynamics influence multiple signalling responses (PI3K lipid products, calcium and Pak phosphorylation) following acute agonist addition or during desensitization. We find that stabilized actin polymer extends the period of receptor desensitization following agonist binding and that actin dynamics rapidly reset receptors from this desensitized state. Spatial differences in actin dynamics may underlie front/back differences in agonist sensitivity in neutrophils.

Indexed as

ActinsAmidesBridged Bicyclo Compounds, HeterocyclicCell LineChemotaxisCytoskeletonDepsipeptidesHumansMyosinsNeutrophilsPhosphorylationPolymerizationPyridinesSignal TransductionThiazolidinesActinsAmidesBridged Bicyclo Compounds, HeterocyclicDepsipeptidesjasplakinolidelatrunculin AMyosinsPyridinesThiazolidinesY 27632actinadaptationcell polaritychemotaxisneutrophilreceptor

Identifiers

PMID24062580
PMCPMC3785960

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.