Evidence map›Paper›PMID 19549683›Full record

ArticleJournal of cell science2009

The beta- and gamma-isoforms of type I PIP5K regulate distinct stages of Ca2+ signaling in mast cells.

Lavanya Vasudevan, Andreas Jeromin, Laura Volpicelli-Daley, Pietro De Camilli, David Holowka, Barbara Baird

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cell science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

29 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. The multifaceted role of PIP2 in leukocyte biology.Cellular and molecular life sciences : CMLS · 2015
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. An Emerging Role for PI5P in T Cell Biology.Frontiers in immunology · 2013
    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

6 authors at 3 institutions in 1 country.

Lavanya VasudevanDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA.
Andreas Jeromin
Laura Volpicelli-Daley
Pietro De Camilli
David Holowka
Barbara Baird
Cornell University · USYale University · USAllen Institute for Brain Science · US

Funding

Yale/NIDA Neuroproteomics Research CenterP30DA018343 · NIDA · YALE UNIVERSITY · PI Marina R Picciotto · 2004 to 2026
$37.1M
INTERACTIVE STRUCTURES AND DYNAMICS OF ANTIGEN RECEPTORSR01AI022449 · NIAID · CORNELL UNIVERSITY ITHACA · PI HOLOWKA, DAVID A · 1985 to 2014
$3.6M
NIAID NIH HHS R01-AI022449NIDA NIH HHS P30 DA018343
6 · The paper itself

Abstract

Crosslinking of IgE receptors by antigen initiates Ca2+ mobilization in mast cells by activating phospholipase-C gamma-mediated hydrolysis of phosphatidylinositol-4,5-bisphosphate [PtdIns(4,5)P2]. The resulting inositol 1,4,5-trisphosphate-mediated Ca2+ release from the endoplasmic reticulum (ER) activates store-operated Ca2+ entry, which is necessary for exocytotic release of inflammatory mediators. To investigate roles for PtdIns(4,5)P2-synthesizing isozymes of the type I phosphatidylinositol 4-phosphate 5-kinase family (PIP5K-I) in mast cell signaling, we compared the ectopic expression of wild-type and catalytically inactive PIP5K-I beta in RBL-2H3 mast cells. Surprisingly, both antigen and thapsigargin-stimulated Ca2+ influx were reduced by overexpression of active PIP5K-I beta, whereas antigen-stimulated Ca2+ release from ER stores was unaffected. Consistent with these results, Ca2+ entry stimulated by antigen or thapsigargin was enhanced by expression of a plasma-membrane-associated inositol polyphosphate 5'-phosphatase, whereas antigen-stimulated Ca2+ release from stores was reduced. To investigate the role of PIP5K-I gamma in antigen-stimulated Ca2+ mobilization, we used bone-marrow-derived mast cells from PIP5K-I gamma(-/-) mice. Antigen-stimulated Ca2+ release from ER stores was substantially reduced in the absence of PIP5K-I gamma, but thapsigargin-mediated Ca2+ entry was unaffected. In summary, PIP5K-I gamma positively regulates antigen-stimulated Ca2+ release from ER stores, whereas PIP5K-I beta negatively regulates store-operated Ca2+ entry, suggesting that these different PIP5K-I isoforms synthesize functionally distinct pools of PtdIns(4,5)P2 at the plasma membrane.

Indexed as

Calcium SignalingAnimalsAntigensBone Marrow CellsCell Line, TumorCell MembraneEndoplasmic ReticulumEnzyme InhibitorsInositol Polyphosphate 5-PhosphatasesIsoenzymesMast CellsMiceMice, KnockoutPhosphatidylinositol 4,5-DiphosphatePhospholipase C gammaPhosphoric Monoester Hydrolases1-phosphatidylinositol-4-phosphate 5-kinaseAntigensEnzyme InhibitorsInositol Polyphosphate 5-PhosphatasesIsoenzymesPhosphatidylinositol 4,5-DiphosphatePhospholipase C gammaPhosphoric Monoester HydrolasesPhosphotransferases (Alcohol Group Acceptor)Receptors, IgERecombinant Fusion ProteinsSarcoplasmic Reticulum Calcium-Transporting ATPasesThapsigargin

Identifiers

PMID19549683
PMCPMC2704887
OpenAlexW2124989505

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.