Evidence map›Paper›PMID 31069116›Full record

ArticleCell death discovery2019

Kremen1-induced cell death is regulated by homo- and heterodimerization.

Iffat Sumia, Alessandra Pierani, Frédéric Causeret

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.5field-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

17 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
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  5. Review
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  8. Increased Kremen2 predicts worse prognosis in colon cancer.Pathology oncology research : POR · 2023
    Article
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  11. Review
  12. Observational
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  17. Synergistic inhibitory effects ofAvicenna journal of phytomedicine
    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

3 authors at 1 institution in 1 country.

Iffat Sumia1Institute of Psychiatry and Neuroscience of Paris, INSERM UMR-S 1266, Université de Paris, Paris, France.
Alessandra Pierani1Institute of Psychiatry and Neuroscience of Paris, INSERM UMR-S 1266, Université de Paris, Paris, France.
Frédéric Causeret1Institute of Psychiatry and Neuroscience of Paris, INSERM UMR-S 1266, Université de Paris, Paris, France.ORCID 0000-0002-0543-4938
University of London Institute in Paris · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In multicellular organisms, cell death pathways allow the removal of abnormal or unwanted cells. Their dysregulation can lead either to excessive elimination or to inappropriate cell survival. Evolutionary constraints ensure that such pathways are strictly regulated in order to restrain their activation to the appropriate context. We have previously shown that the transmembrane receptor Kremen1 behaves as a dependence receptor, triggering cell death unless bound to its ligand Dickkopf1. In this study, we reveal that Kremen1 apoptotic signaling requires homodimerization of the receptor. Dickkopf1 binding inhibits Kremen1 multimerization and alleviates cell death, whereas forced dimerization increases apoptotic signaling. Furthermore, we show that Kremen2, a paralog of Kremen1, which bears no intrinsic apoptotic activity, binds and competes with Kremen1. Consequently, Kremen2 is a very potent inhibitor of Kremen1-induced cell death. Kremen1 was proposed to act as a tumor suppressor, preventing cancer cell survival in a ligand-poor environment. We found that

Indexed as

ApoptosisCancerCell deathCell signalling

Identifiers

PMID31069116
PMCPMC6494814
OpenAlexW2943204476

What OpenQuestion holds

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LicenceCC BY
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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.