Evidence map›Paper›PMID 26569406›Full record

ArticlePloS one2015

The Bulk of Autotaxin Activity Is Dispensable for Adult Mouse Life.

Aggeliki Katsifa, Eleanna Kaffe, Nefeli Nikolaidou-Katsaridou, Aris N Economides, Susan Newbigging, Colin McKerlie, Vassilis Aidinis

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

40 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Autotaxin Expression in the Uterus of Cycling Rats.Development & reproduction · 2024
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Designing Dual Inhibitors of Autotaxin-LPAR GPCR Axis.Molecules (Basel, Switzerland) · 2022
    Review
  13. Autotaxin Has a Negative Role in Systemic Inflammation.International journal of molecular sciences · 2022
    Article
  14. Article
  15. Article
  16. Design and Development of Autotaxin Inhibitors.Pharmaceuticals (Basel, Switzerland) · 2021
    Review
  17. Article
  18. Autotaxin-LPA-LPP3 Axis in Energy Metabolism and Metabolic Disease.International journal of molecular sciences · 2021
    Review
  19. Article
  20. Review
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

7 authors at 4 institutions in 3 countries.

Aggeliki KatsifaDivision of Immunology, Biomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Eleanna KaffeDivision of Immunology, Biomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Nefeli Nikolaidou-KatsaridouDivision of Immunology, Biomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Aris N EconomidesGenome Engineering Technologies Group and Skeletal Diseases TFA Group, Regeneron Pharmaceuticals Inc., Tarrytown, New York, United States of America.
Susan NewbiggingPhysiology and Experimental Medicine Research Program, the Hospital for Sick Children, Center for Phenogenomics, Toronto, Canada.
Colin McKerliePhysiology and Experimental Medicine Research Program, the Hospital for Sick Children, Center for Phenogenomics, Toronto, Canada.
Vassilis AidinisDivision of Immunology, Biomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Alexander Fleming Biomedical Sciences Research Center · GRHospital for Sick Children · CARegeneron (United States) · USSickKids Foundation · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autotaxin (ATX, Enpp2) is a secreted lysophospholipase D catalysing the production of lysophosphatidic acid, a pleiotropic growth factor-like lysophospholipid. Increased ATX expression has been detected in a number of chronic inflammatory diseases and different types of cancer, while genetic interventions have proven a role for ATX in disease pathogenesis. Therefore, ATX has emerged as a potential drug target and a large number of ATX inhibitors have been developed exhibiting promising therapeutic potential. However, the embryonic lethality of ATX null mice and the ubiquitous expression of ATX and LPA receptors in adult life question the suitability of ATX as a drug target. Here we show that inducible, ubiquitous genetic deletion of ATX in adult mice, as well as long-term potent pharmacologic inhibition, are well tolerated, alleviating potential toxicity concerns of ATX therapeutic targeting.

Indexed as

AgingAnimalsBenzoxazolesEnzyme ActivationIntegrasesLysophospholipase DMice, Inbred C57BLPhosphoric Diester HydrolasesPiperazinesTamoxifen6-(3-(piperazin-1-yl)propanoyl)benzo(d)oxazol-2(3H)-oneBenzoxazolesCre recombinaseIntegrasesLysophospholipase DPhosphoric Diester HydrolasesPiperazinesTamoxifen

Identifiers

PMID26569406
PMCPMC4646642
OpenAlexW2274594132

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.