Evidence map›Paper›PMID 30446682›Full record

ArticleScientific reports2018

DLK proteins modulate NOTCH signaling to influence a brown or white 3T3-L1 adipocyte fate.

María-Luisa Nueda, María-Julia González-Gómez, María-Milagros Rodríguez-Cano, Eva-María Monsalve, María José M Díaz-Guerra, Beatriz Sánchez-Solana, Jorge Laborda, Victoriano Baladrón

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.4field-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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

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  19. Studying the NOTCH Signaling Pathway Activation in Kidney Biopsies.Methods in molecular biology (Clifton, N.J.) · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

María-Luisa NuedaÁrea de Bioquímica y Biología Molecular, Dpto. Química Inorgánica y Bioquímica, Facultad de Farmacia/CRIB/Unidad de Biomedicina, Universidad de Castilla-La Mancha/CSIC. C/Almansa 14, 02008, Albacete, Spain.
María-Julia González-GómezÁrea de Bioquímica y Biología Molecular, Dpto. Química Inorgánica y Bioquímica, Facultad de Farmacia/CRIB/Unidad de Biomedicina, Universidad de Castilla-La Mancha/CSIC. C/Almansa 14, 02008, Albacete, Spain.
María-Milagros Rodríguez-CanoÁrea de Bioquímica y Biología Molecular, Dpto. Química Inorgánica y Bioquímica, Facultad de Farmacia/CRIB/Unidad de Biomedicina, Universidad de Castilla-La Mancha/CSIC. C/Almansa 14, 02008, Albacete, Spain.
Eva-María MonsalveÁrea de Bioquímica y Biología Molecular, Dpto. Química Inorgánica, Orgánica y Bioquímica, Facultad de Medicina de Albacete/CRIB/Unidad de Biomedicina, Universidad de Castilla-La Mancha/CSIC, C/Almansa 14, 02008, Albacete, Spain.
María José M Díaz-GuerraÁrea de Bioquímica y Biología Molecular, Dpto. Química Inorgánica, Orgánica y Bioquímica, Facultad de Medicina de Albacete/CRIB/Unidad de Biomedicina, Universidad de Castilla-La Mancha/CSIC, C/Almansa 14, 02008, Albacete, Spain.
Beatriz Sánchez-SolanaLaboratory of Cellular Oncology, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, MD, USA.
Jorge LabordaÁrea de Bioquímica y Biología Molecular, Dpto. Química Inorgánica y Bioquímica, Facultad de Farmacia/CRIB/Unidad de Biomedicina, Universidad de Castilla-La Mancha/CSIC. C/Almansa 14, 02008, Albacete, Spain.
Victoriano BaladrónÁrea de Bioquímica y Biología Molecular, Dpto. Química Inorgánica, Orgánica y Bioquímica, Facultad de Medicina de Albacete/CRIB/Unidad de Biomedicina, Universidad de Castilla-La Mancha/CSIC, C/Almansa 14, 02008, Albacete, Spain. Victoriano.Baladron@uclm.es.ORCID http://orcid.org/0000-0003-4574-8760
University of Castilla-La Mancha · ESNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of NOTCH signaling in adipogenesis is highly controversial, with data indicating null, positive or negative effects on this differentiation process. We hypothesize that these contradictory results could be due to the different global NOTCH signaling levels obtained in different experimental settings, because of a specific modulation of NOTCH receptors' activity by their ligands. We have previously demonstrated that DLK1 and DLK2, two non-canonical NOTCH1 ligands that inhibit NOTCH1 signaling in a dose-dependent manner, modulate the adipogenesis process of 3T3-L1 preadipocytes. In this work, we show that over-expression of any of the four NOTCH receptors enhanced adipogenesis of 3T3-L1 preadipocytes. We also determine that DLK proteins inhibit not only the activity of NOTCH1, but also the activity of NOTCH2, 3 and 4 receptors to different degrees. Interestingly, we have observed, by different approaches, that NOTCH1 over-expression seems to stimulate the differentiation of 3T3-L1 cells towards a brown-like adipocyte phenotype, whereas cells over-expressing NOTCH2, 3 or 4 receptors or DLK proteins would rather differentiate towards a white-like adipocyte phenotype. Finally, our data also demonstrate a complex feed-back mechanism involving Notch and Dlk genes in the regulation of their expression, which suggest that a precise level of global NOTCH expression and NOTCH-dependent transcriptional activity of specific targets could be necessary to determine the final phenotype of 3T3-L1 adipocytes.

Identifiers

PMID30446682
PMCPMC6240076
OpenAlexW2901642625

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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.