Evidence map›Paper›PMID 29333002›Full record

ReviewMediators of inflammation2017

S1P Lyase Regulation of Thymic Egress and Oncogenic Inflammatory Signaling.

Ashok Kumar, Jesus Zamora-Pineda, Emilie Degagné, Julie D Saba

Open access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Regulation of cellular and systemic sphingolipid homeostasis.Nature reviews. Molecular cell biology · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. The Role of Sphingolipids in Cancer Immunotherapy.International journal of molecular sciences · 2021
    Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  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

4 authors at 2 institutions in 2 countries.

Ashok KumarDepartment of Biochemistry, All India Institute of Medical Sciences (AIIMS) Bhopal, Madhya Pradesh 462020, India.
Jesus Zamora-PinedaChildren's Hospital Oakland Research Institute and UCSF Benioff Children's Hospital Oakland, 5700 Martin Luther King Jr. Way, Oakland, CA 94609, USA.
Emilie DegagnéChildren's Hospital Oakland Research Institute and UCSF Benioff Children's Hospital Oakland, 5700 Martin Luther King Jr. Way, Oakland, CA 94609, USA.
Julie D SabaChildren's Hospital Oakland Research Institute and UCSF Benioff Children's Hospital Oakland, 5700 Martin Luther King Jr. Way, Oakland, CA 94609, USA.ORCID 0000-0002-4894-919X
UCSF Benioff Children's Hospital · USAll India Institute of Medical Sciences Bhopal · IN

Funding

S1P Lyase in colon cancerR01CA129438 · NCI · CHILDREN'S HOSPITAL & RES CTR AT OAKLAND · PI SABA, JULIE D · 2007 to 2017
$3.2M
NCI NIH HHS R01 CA129438
6 · The paper itself

Abstract

Sphingosine-1-phosphate (S1P) is a potent lipid signaling molecule that regulates pleiotropic biological functions including cell migration, survival, angiogenesis, immune cell trafficking, inflammation, and carcinogenesis. It acts as a ligand for a family of cell surface receptors. S1P concentrations are high in blood and lymph but low in tissues, especially the thymus and lymphoid organs. S1P chemotactic gradients are essential for lymphocyte egress and other aspects of physiological cell trafficking. S1P is irreversibly degraded by S1P lyase (SPL). SPL regulates lymphocyte trafficking, inflammation and other physiological and pathological processes. For example, SPL located in thymic dendritic cells acts as a metabolic gatekeeper that controls the normal egress of mature T lymphocytes from the thymus into the circulation, whereas SPL deficiency in gut epithelial cells promotes colitis and colitis-associated carcinogenesis (CAC). Recently, we identified a complex syndrome comprised of nephrosis, adrenal insufficiency, and immunological defects caused by inherited mutations in human

Indexed as

Aldehyde-LyasesAnimalsCarcinogenesisCell MovementDendritic CellsHumansInflammationInflammation MediatorsLysophospholipidsModels, BiologicalMutationSignal TransductionSphingosineT-LymphocytesAldehyde-LyasesInflammation MediatorsLysophospholipidsSGPL1 protein, humanSphingosinesphingosine 1-phosphatesphingosine 1-phosphate lyase (aldolase)

Identifiers

PMID29333002
PMCPMC5733215
OpenAlexW2775102332

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.