Evidence map›Paper›PMID 27789627›Full record

ArticleDevelopment (Cambridge, England)2016

Filamin A- and formin 2-dependent endocytosis regulates proliferation via the canonical Wnt pathway.

Gewei Lian, Markus Dettenhofer, Jie Lu, Michael Downing, Anjen Chenn, Timothy Wong, Volney Sheen

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.1field-weighted citation impact, top 14% 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, 45 citations in OpenAlex.

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  17. Specialized cytonemes induce self-organization of stem cells.Proceedings of the National Academy of Sciences of the United States of America · 2020
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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

7 authors at 3 institutions in 2 countries.

Gewei LianDepartment of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02115, USA.
Markus DettenhoferCentral European Institute of Technology, Žerotínovo nám. 9, Brno 601 77, Czech Republic.
Jie LuDepartment of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02115, USA.
Michael DowningDepartment of Pathology, University of Illinois College of Medicine, Chicago, IL 60612, USA.
Anjen ChennDepartment of Pathology, University of Illinois College of Medicine, Chicago, IL 60612, USA.
Timothy WongDepartment of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02115, USA.
Volney SheenDepartment of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02115, USA vsheen@bidmc.harvard.edu.ORCID 0000-0002-7931-8200
Beth Israel Deaconess Medical Center · USIllinois College · USCentral European Institute of Technology · CZ

Funding

Apical Abscission and Periventricular Heterotopia: A common basis for diseaseR01NS092062 · NINDS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI FERLAND, RUSSELL JAMES, SHEEN, VOLNEY L · 2015 to 2019
$1.8M
NINDS NIH HHS R01 NS092062
6 · The paper itself

Abstract

Actin-associated proteins regulate multiple cellular processes, including proliferation and differentiation, but the molecular mechanisms underlying these processes are unclear. Here, we report that the actin-binding protein filamin A (FlnA) physically interacts with the actin-nucleating protein formin 2 (Fmn2). Loss of FlnA and Fmn2 impairs proliferation, thereby generating multiple embryonic phenotypes, including microcephaly. FlnA interacts with the Wnt co-receptor Lrp6. Loss of FlnA and Fmn2 impairs Lrp6 endocytosis, downstream Gsk3β activity, and β-catenin accumulation in the nucleus. The proliferative defect in Flna and Fmn2 null neural progenitors is rescued by inhibiting Gsk3β activity. Our findings thus reveal a novel mechanism whereby actin-associated proteins regulate proliferation by mediating the endocytosis and transportation of components in the canonical Wnt pathway. Moreover, the Fmn2-dependent signaling in this pathway parallels that seen in the non-canonical Wnt-dependent regulation of planar cell polarity through the Formin homology protein Daam. These studies provide evidence for integration of actin-associated processes in directing neuroepithelial proliferation.

Indexed as

Animalsbeta CateninCell DifferentiationCell LineCell MembraneCell ProliferationEndocytosisFilaminsForminsGlycogen Synthase Kinase 3 betaHEK293 CellsHumansLow Density Lipoprotein Receptor-Related Protein-6MiceMice, KnockoutMicrocephalybeta CateninFilaminsFlnA protein, mouseformin 2 protein, mouseForminsGlycogen Synthase Kinase 3 betaLow Density Lipoprotein Receptor-Related Protein-6Lrp6 protein, mouseMicrofilament ProteinsNerve Tissue ProteinsNuclear ProteinsWnt ProteinsDifferentiationEndocytosisFilaminForminLrp6Neural progenitorProliferationVesicle trafficking

Identifiers

PMID27789627
PMCPMC5201043
OpenAlexW2544914745

What OpenQuestion holds

Textmetadata
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.