Evidence map›Paper›PMID 32894219›Full record

ArticleeLife2020

Novel C1q receptor-mediated signaling controls neural stem cell behavior and neurorepair.

Francisca Benavente, Katja M Piltti, Mitra J Hooshmand, Aileen A Nava, Anita Lakatos, Brianna G Feld, Dana Creasman, Paul D Gershon, Aileen Anderson

Open access · goldAbstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

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  9. [C1q-neutralizing antibodies improves postpartum depressive-like behaviors in mice by regulating the C1q/C3 pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
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  11. Astrocytic EphA4 signaling is important for the elimination of excitatory synapses in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  15. Article
  16. C1q is elevated during chronicFrontiers in immunology · 2024
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  18. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Francisca BenaventeSue and Bill Gross Stem Cell Research Center, Irvine, United States.ORCID https://orcid.org/0000-0001-8245-2673
Katja M PilttiSue and Bill Gross Stem Cell Research Center, Irvine, United States.
Mitra J HooshmandSue and Bill Gross Stem Cell Research Center, Irvine, United States.ORCID http://orcid.org/0000-0001-6159-6934
Aileen A NavaSue and Bill Gross Stem Cell Research Center, Irvine, United States.ORCID http://orcid.org/0000-0002-2053-6713
Anita LakatosSue and Bill Gross Stem Cell Research Center, Irvine, United States.
Brianna G FeldSue and Bill Gross Stem Cell Research Center, Irvine, United States.
Dana CreasmanSue and Bill Gross Stem Cell Research Center, Irvine, United States.
Paul D GershonDepartment of Physical Medicine and Rehabilitation, Irvine, United States.
Aileen AndersonSue and Bill Gross Stem Cell Research Center, Irvine, United States.ORCID https://orcid.org/0000-0002-8203-8891
University of California, Irvine · USCalifornia State University, Long Beach · USUniversidad del Desarrollo · CL

Funding

LTQ Velos Pro mass spectrometer with ETD and other optionsS10OD016328 · OD · UNIVERSITY OF CALIFORNIA-IRVINE · PI GERSHON, PAUL D · 2013 to 2013
$374k
NIH HHS 1S10OD016328-01NIH HHS S10 OD016328
6 · The paper itself

Abstract

C1q plays a key role as a recognition molecule in the immune system, driving autocatalytic complement cascade activation and acting as an opsonin. We have previously reported a non-immune role of complement C1q modulating the migration and fate of human neural stem cells (hNSC); however, the mechanism underlying these effects has not yet been identified. Here, we show for the first time that C1q acts as a functional hNSC ligand, inducing intracellular signaling to control cell behavior. Using an unbiased screening strategy, we identified five transmembrane C1q signaling/receptor candidates in hNSC (CD44, GPR62, BAI1, c-MET, and ADCY5). We further investigated the interaction between C1q and CD44 , demonstrating that CD44 mediates C1q induced hNSC signaling and chemotaxis in vitro, and hNSC migration and functional repair in vivo after spinal cord injury. These results reveal a receptor-mediated mechanism for C1q modulation of NSC behavior and show that modification of C1q receptor expression can expand the therapeutic window for hNSC transplantation.

Indexed as

AnimalsCell DifferentiationCells, CulturedCell TransplantationComplement C1qHyaluronan ReceptorsMembrane GlycoproteinsMiceNeural Stem CellsReceptors, ComplementSignal TransductionSpinal Cord Injuriescomplement 1q receptorComplement C1qHyaluronan ReceptorsMembrane GlycoproteinsReceptors, Complementcomplement C1qmouseneural stem cell transplantsregenerative medicinespinal cord injurystem cells

Identifiers

PMID32894219
PMCPMC7476762
OpenAlexW3083015011

What OpenQuestion holds

Textmetadata
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.