Evidence map›Paper›PMID 16201965›Full record

ArticleThe Biochemical journal2006

Regulation of the sphingosine-recycling pathway for ceramide generation by oxidative stress, and its role in controlling c-Myc/Max function.

Iyad Sultan, Can E Senkal, Suriyan Ponnusamy, Jacek Bielawski, Zdzislaw Szulc, Alicja Bielawska, Yusuf A Hannun, Besim Ogretmen

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.4field-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

28 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Sphingolipids and Lipoproteins in Health and Metabolic Disorders.Trends in endocrinology and metabolism: TEM · 2017
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Ceramide signaling in mammalian epidermis.Biochimica et biophysica acta · 2014
    Review
  11. Article
  12. Article
  13. Article
  14. Sphingolipids in obesity, type 2 diabetes, and metabolic disease.Handbook of experimental pharmacology · 2013
    Review
  15. Review
  16. Article
  17. Article
  18. Neutral sphingomyelinase 2: a novel target in cigarette smoke-induced apoptosis and lung injury.American journal of respiratory cell and molecular biology · 2011
    Article
  19. Review
  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

8 authors at 1 institution in 1 country.

Iyad SultanDepartment of Biochemistry and Molecular Biology, Medical University of South Carolina, 173 Ashley Avenue, Charleston, SC 29425, USA.
Can E Senkal
Suriyan Ponnusamy
Jacek Bielawski
Zdzislaw Szulc
Alicja Bielawska
Yusuf A Hannun
Besim Ogretmen
Medical University of South Carolina · US

Funding

Regulation of Telomerase by Sphingolipid Signaling in Lung CancerR01CA088932 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI OGRETMEN, BESIM · 2002 to 2017
$3.3M
NCI NIH HHS CA-88932NCI NIH HHS R01 CA088932
6 · The paper itself

Abstract

In the present study, the regulation of the sphingosine-recycling pathway in A549 human lung adenocarcinoma cells by oxidative stress was investigated. The generation of endogenous long-chain ceramide in response to exogenous C6-cer (C6-ceramide), which is FB1 (fumonisin B1)-sensitive, was employed to probe the sphingosine-recycling pathway. The data showed that ceramide formation via this pathway was significantly blocked by GSH and NAC (N-acetylcysteine) whereas it was enhanced by H2O2, as detected by both palmitate labelling and HPLC/MS. Similar data were also obtained using a novel approach that measures the incorporation of 17Sph (sphingosine containing 17 carbons) of 17C6-cer (C6-cer containing a 17Sph backbone) into long-chain 17C16-cer in cells by HPLC/MS, which was significantly decreased and increased in response to GSH and H2O2 respectively. TNF (tumour necrosis factor)-a, which decreases the levels of endogenous GSH, increased the generation of C16-cer in response to C6-cer, and this was blocked by exogenous GSH or NAC, or by the overexpression of TPx I (thioredoxin peroxidase I), an enzyme that reduces the generation of intracellular ROS (reactive oxygen species). Additional data showed that ROS regulated both the deacylation and reacylation steps of C6-cer. At a functional level, C6-cer inhibited the DNA-binding function of the c-Myc/Max oncogene. Inhibition of the generation of longchain ceramide in response to C6-cer by FB1 or NAC significantly blocked the modulation of the c-Myc/Max function. These data demonstrate that the sphingosine-recycling pathway for the generation of endogenous long-chain ceramide in response to exogenous C6-cer is regulated by ROS, and plays an important biological role in controlling c-Myc function.

Indexed as

Oxidative StressAcylationBasic-Leucine Zipper Transcription FactorsCell Line, TumorCeramidesGene Expression RegulationGolgi ApparatusHumansProtein BindingProto-Oncogene Proteins c-mycReactive Oxygen SpeciesSphingosineSubstrate SpecificityThioredoxin-Disulfide ReductaseThioredoxin Reductase 1Time FactorsBasic-Leucine Zipper Transcription FactorsCeramidesMyc associated factor XProto-Oncogene Proteins c-mycReactive Oxygen SpeciesSphingosineThioredoxin-Disulfide ReductaseThioredoxin Reductase 1Tumor Necrosis Factor-alphaTXNRD1 protein, human

Identifiers

PMID16201965
PMCPMC1360701
OpenAlexW2075220915

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.