Evidence map›Paper›PMID 28852127›Full record

ArticleScientific reports2017

BBS4 regulates the expression and secretion of FSTL1, a protein that participates in ciliogenesis and the differentiation of 3T3-L1.

Victoria Prieto-Echagüe, Sukanya Lodh, Laura Colman, Natalia Bobba, Leonardo Santos, Nicholas Katsanis, Carlos Escande, Norann A Zaghloul, Jose L Badano

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Follistatin like-1 (Adipocyte · 2024
    Article
  2. Article
  3. Role of follistatin-like protein 1 in liver diseases.Experimental biology and medicine (Maywood, N.J.) · 2023
    Review
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  15. Follistatin-like 1 in development and human diseases.Cellular and molecular life sciences : CMLS · 2018
    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

9 authors at 3 institutions in 2 countries.

Victoria Prieto-EchagüeHuman Molecular Genetics Laboratory, Institut Pasteur de Montevideo, Mataojo 2020, Montevideo, CP11400, Uruguay.ORCID 0000-0001-9924-9591
Sukanya LodhDivision of Endocrinology, Diabetes, and Nutrition, University of Maryland School of Medicine, Baltimore, MD, 21201, USA.
Laura ColmanINDICyO Institutional Program, Institut Pasteur de Montevideo, Mataojo 2020, Montevideo, CP11400, Uruguay.
Natalia BobbaINDICyO Institutional Program, Institut Pasteur de Montevideo, Mataojo 2020, Montevideo, CP11400, Uruguay.
Leonardo SantosINDICyO Institutional Program, Institut Pasteur de Montevideo, Mataojo 2020, Montevideo, CP11400, Uruguay.
Nicholas KatsanisDepartment of Cell Biology and Center for Human Disease Modeling, Duke University Medical Center, Durham, NC, 27710, USA.
Carlos EscandeINDICyO Institutional Program, Institut Pasteur de Montevideo, Mataojo 2020, Montevideo, CP11400, Uruguay.
Norann A ZaghloulDivision of Endocrinology, Diabetes, and Nutrition, University of Maryland School of Medicine, Baltimore, MD, 21201, USA.
Jose L BadanoHuman Molecular Genetics Laboratory, Institut Pasteur de Montevideo, Mataojo 2020, Montevideo, CP11400, Uruguay. jbadano@pasteur.edu.uy.ORCID 0000-0002-0706-8652
Institut Pasteur de Montevideo · UYUniversity of Maryland, Baltimore · USDuke University · US

Funding

Research BaseP30DK072488 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI MITCHELL, BRAXTON D, TAYLOR, SIMEON I. · 2005 to 2019
$17.3M
Genetic and Functional Studies of Human Ciliary SyndromesR01DK072301 · NIDDK · LURIE CHILDREN'S HOSPITAL OF CHICAGO · PI DAVIS, ERICA ELLEN · 2005 to 2022
$7.2M
Basal body regulation of glucose homeostasisR01DK102001 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI MITCHELL, BRAXTON D · 2014 to 2018
$1.7M
The Role of Basal Bodies in Wnt SignalingR01GM121317 · NIGMS · LURIE CHILDREN'S HOSPITAL OF CHICAGO · PI DAVIS, ERICA ELLEN · 2016 to 2019
$1.7M
NIDDK NIH HHS P30 DK072488NIDDK NIH HHS R01 DK072301NIDDK NIH HHS R01 DK102001NIGMS NIH HHS R01 GM121317
6 · The paper itself

Abstract

Bardet-Biedl syndrome is a model ciliopathy. Although the characterization of BBS proteins has evidenced their involvement in cilia, extraciliary functions for some of these proteins are also being recognized. Importantly, understanding both cilia and cilia-independent functions of the BBS proteins is key to fully dissect the cellular basis of the syndrome. Here we characterize a functional interaction between BBS4 and the secreted protein FSTL1, a protein linked to adipogenesis and inflammation among other functions. We show that BBS4 and cilia regulate FSTL1 mRNA levels, but BBS4 also modulates FSTL1 secretion. Moreover, we show that FSTL1 is a novel regulator of ciliogenesis thus underscoring a regulatory loop between FSTL1 and cilia. Finally, our data indicate that BBS4, cilia and FSTL1 are coordinated during the differentiation of 3T3-L1 cells and that FSTL1 plays a role in this process, at least in part, by modulating ciliogenesis. Therefore, our findings are relevant to fully understand the development of BBS-associated phenotypes such as obesity.

Indexed as

Gene Expression Regulation3T3-L1 CellsAdipocytesAdipogenesisAnimalsCell DifferentiationCiliaFollistatin-Related ProteinsGene Knockdown TechniquesIntracellular SpaceMiceMicrotubule-Associated ProteinsProteinsBBS4 protein, humanFollistatin-Related ProteinsFSTL1 protein, humanMicrotubule-Associated ProteinsProteins

Identifiers

PMID28852127
PMCPMC5575278
OpenAlexW2746718543

What OpenQuestion holds

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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.