Evidence map›Paper›PMID 32161116›Full record

ArticleThe Journal of biological chemistry2020

Repression of sphingosine kinase (SK)-interacting protein (SKIP) in acute myeloid leukemia diminishes SK activity and its re-expression restores SK function.

Essam A Ghazaly, Farideh Miraki-Moud, Paul Smith, Chathunissa Gnanaranjan, Lola Koniali, Adedayo Oke, Marwa H Saied, Robert Petty, Janet Matthews, Randal Stronge and 4 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Subcellular Stress Markers in Epithelial Ovarian Cancer.International journal of molecular sciences · 2025
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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

14 authors at 3 institutions in 1 country.

Essam A GhazalyCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ, United Kingdom.
Farideh Miraki-MoudCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ, United Kingdom; Institute of Cancer Research, Sutton, London, United Kingdom.
Paul SmithCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ, United Kingdom.
Chathunissa GnanaranjanCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ, United Kingdom.
Lola KonialiCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ, United Kingdom.
Adedayo OkeCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ, United Kingdom.
Marwa H SaiedCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ, United Kingdom.
Robert PettyCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ, United Kingdom.
Janet MatthewsCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ, United Kingdom.
Randal StrongeInstitute of Cancer Research, Sutton, London, United Kingdom; Department of Haematology, Royal Marsden Hospital, Sutton, United Kingdom.
Simon P JoelCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ, United Kingdom.
Bryan D YoungCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ, United Kingdom.
John GribbenCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ, United Kingdom.
David C TaussigCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, London EC1M 6BQ, United Kingdom; Institute of Cancer Research, Sutton, London, United Kingdom; Department of Haematology, Royal Marsden Hospital, Sutton, United Kingdom. Electronic address: e.a.ghazaly@qmul.ac.uk.
Queen Mary University of London · GBInstitute of Cancer Research · GBRoyal Marsden NHS Foundation Trust · GB

Funding

Department of Health
6 · The paper itself

Abstract

Previous studies have shown that sphingosine kinase interacting protein (SKIP) inhibits sphingosine kinase (SK) function in fibroblasts. SK phosphorylates sphingosine producing the potent signaling molecule sphingosine-1-phosphate (S1P).

Indexed as

Adaptor Proteins, Signal TransducingCeramidesHumansK562 CellsLeukemia, Myeloid, AcutePhosphotransferases (Alcohol Group Acceptor)Sphingosine KinaseTumor Cells, CulturedAdaptor Proteins, Signal TransducingCeramidesPhosphotransferases (Alcohol Group Acceptor)Sphingosine KinaseSPHKAP protein, humanAcute myeloid leukemiacell signalingceramidechemotherapycytarabinehypermethylationleukemialipid metabolismsphingolipidsphingosine-1-phosphate (S1P)sphingosine kinase interacting proteinSphingosine kinase (SphK)

Identifiers

PMID32161116
PMCPMC7170527
OpenAlexW3011428406

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.