Evidence map›Paper›PMID 27551447›Full record

ArticleCell death discovery2015

Stereospecific induction of apoptosis in tumor cells via endogenous C16-ceramide and distinct transcripts.

M Blaess, H P Le, R A Claus, M Kohl, H-P Deigner

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.3field-weighted citation impact, top 36% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

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  8. CInternational journal of molecular sciences · 2019
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  9. 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

5 authors at 2 institutions in 1 country.

M BlaessCenter for Sepsis Control and Care (CSCC), Jena University Hospital, Erlanger Allee 101, D-07747 Jena, Germany; Clinic for Anaesthesiology and Intensive Care, Jena University Hospital, Erlanger Allee 101, D-07747 Jena, Germany.
H P LeMedical and Life Sciences Faculty, Furtwangen University , Jakob-Kienzle-Strasse 17, D-78054 Villingen-Schwenningen, Germany.
R A ClausCenter for Sepsis Control and Care (CSCC), Jena University Hospital, Erlanger Allee 101, D-07747 Jena, Germany; Clinic for Anaesthesiology and Intensive Care, Jena University Hospital, Erlanger Allee 101, D-07747 Jena, Germany.
M KohlMedical and Life Sciences Faculty, Furtwangen University , Jakob-Kienzle-Strasse 17, D-78054 Villingen-Schwenningen, Germany.
H-P DeignerMedical and Life Sciences Faculty, Furtwangen University, Jakob-Kienzle-Strasse 17, D-78054 Villingen-Schwenningen, Germany; Fraunhofer Institute IZI, Leipzig, EXIM Department, Schillingallee 68, D-18057 Rostock, Germany.
Furtwangen University · DEJena University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Concentration and distribution of individual endogenous ceramide species is crucial for apoptosis induction in response to various stimuli. Exogenous ceramide analogs induce apoptosis and can in turn modify the composition/concentrations of endogenous ceramide species and associated signaling. In this study, we show here that the elevation of endogenous C16-ceramide levels is a common feature of several known apoptosis-inducing triggers like mmLDL, TNF-alpha, H2O2 and exogenous C6-ceramide. Vice versa apoptosis requires elevation of endogenous C16-ceramide levels in cells. Enantiomers of a synthetic ceramide analog HPL-1RS36N have been developed as probes and vary in their capacity to inducing apoptosis in macrophages and HT-29 cells. Apoptosis induction by the two synthetic ceramide analogs HPL-39N and HPL-1R36N correlates with generation of cellular C16-ceramide concentration. In contrast to the S-enantiomer HPL-1S36N, the R-enantiomer HPL-1R36N shows significant effects on the expression of distinct genes known to be involved in cell cycle, cell growth and cell death (CXCL10, CCL5 and TNF-alpha), similarly on apoptosis induction. Enantioselective effects on transcription induced by metabolically stable synthetic probes provide clues on molecular mechanisms of ceramide-induced signaling, as well as leads for future anti-cancer agents.

Identifiers

PMID27551447
PMCPMC4979478
OpenAlexW2534857489

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.