Evidence map›Paper›PMID 11907258›Full record

ArticleMolecular biology of the cell2002

Genetic ablation of phosphatidylinositol transfer protein function in murine embryonic stem cells.

James G Alb, Scott E Phillips, Kathleen Rostand, Xiaoxia Cui, Jef Pinxteren, Laura Cotlin, Timothy Manning, Shuling Guo, John D York, Harald Sontheimer and 2 more

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Courier service for phosphatidylinositol: PITPs deliver on demand.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2021
    Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Repression of phosphatidylinositol transfer protein α ameliorates the pathology of Duchenne muscular dystrophy.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
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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

12 authors at 6 institutions in 3 countries.

James G AlbDepartment of Cell and Developmental Biology, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7090, USA.
Scott E Phillips
Kathleen Rostand
Xiaoxia Cui
Jef Pinxteren
Laura Cotlin
Timothy Manning
Shuling Guo
John D York
Harald Sontheimer
James F Collawn
Vytas A Bankaitis
Institute of Cell Biology · UAUniversity of North Carolina at Chapel Hill · USUniversity of Alabama at Birmingham · USDuke University Hospital · USHoward Hughes Medical Institute · USUniversity College London · GB

Funding

PTDINS TRANSFER PROTEIN FUNCTION AND NEURODEGENERATIONR01NS037723 · NINDS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BANKAITIS, VYTAS A · 1998 to 2007
$2.2M
Ptdins Transfer Protein Function and NeurodegenerationR56NS037723 · NINDS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BANKAITIS, VYTAS A · 2010 to 2010
$370k
NINDS NIH HHS NS37723NINDS NIH HHS R01 NS037723NINDS NIH HHS R56 NS037723
6 · The paper itself

Abstract

Phosphatidylinositol transfer proteins (PITPs) regulate the interface between signal transduction, membrane-trafficking, and lipid metabolic pathways in eukaryotic cells. The best characterized mammalian PITPs are PITP alpha and PITP beta, two highly homologous proteins that are encoded by distinct genes. Insights into PITP alpha and PITP beta function in mammalian systems have been gleaned exclusively from cell-free or permeabilized cell reconstitution and resolution studies. Herein, we report for the first time the use of genetic approaches to directly address the physiological functions of PITP alpha and PITP beta in murine cells. Contrary to expectations, we find that ablation of PITP alpha function in murine cells fails to compromise growth and has no significant consequence for bulk phospholipid metabolism. Moreover, the data show that PITP alpha does not play an obvious role in any of the cellular activities where it has been reconstituted as an essential stimulatory factor. These activities include protein trafficking through the constitutive secretory pathway, endocytic pathway function, biogenesis of mast cell dense core secretory granules, and the agonist-induced fusion of dense core secretory granules to the mast cell plasma membrane. Finally, the data demonstrate that PITP alpha-deficient cells not only retain their responsiveness to bulk growth factor stimulation but also retain their pluripotency. In contrast, we were unable to evict both PITP beta alleles from murine cells and show that PITP beta deficiency results in catastrophic failure early in murine embryonic development. We suggest that PITP beta is an essential housekeeping PITP in murine cells, whereas PITP alpha plays a far more specialized function in mammals than that indicated by in vitro systems that show PITP dependence.

Indexed as

AnimalsBinding SitesCarrier ProteinsCell LineCell SurvivalEndocytosisExocytosisFlow CytometryGene TargetingGenotypeImmunoglobulin EMast CellsMembrane ProteinsMiceMice, NudePhospholipidsCarrier ProteinsImmunoglobulin EMembrane ProteinsPhospholipidsPhospholipid Transfer ProteinsProtein IsoformsReceptors, Transferrin

Identifiers

PMID11907258
PMCPMC99595
OpenAlexW2098779810

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.