Evidence map›Paper›PMID 22349703›Full record

ArticleJournal of cell science2012

Differential regulation of myosin X movements by its cargos, DCC and neogenin.

Yu Liu, Yun Peng, Peng-Gao Dai, Quan-Sheng Du, Lin Mei, Wen-Cheng Xiong

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cell science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Myosin X Interaction with KIF13B, a Crucial Pathway for Netrin-1-Induced Axonal Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  3. Article
  4. Lack of Myosin X Enhances Osteoclastogenesis and Increases Cell Surface Unc5b in Osteoclast-Lineage Cells.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019
    Article
  5. Revisiting Netrin-1: One Who Guides (Axons).Frontiers in cellular neuroscience · 2018
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. 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

6 authors at 3 institutions in 2 countries.

Yu LiuInstitute of Molecular Medicine & Genetics and Department of Neurology, Medical College of Georgia, Georgia Health Sciences University, Augusta, GA 30912, USA.
Yun Peng
Peng-Gao Dai
Quan-Sheng Du
Lin Mei
Wen-Cheng Xiong
Augusta University · USCharlie Norwood VA Medical Center · USZhongnan Hospital of Wuhan University · CN

Funding

Molecular Mechanisms Underlying Axon PathfindingR01NS060648 · NINDS · AUGUSTA UNIVERSITY · PI XIONG, WEN-CHENG · 2008 to 2012
$1.6M
NINDS NIH HHS NS060648NINDS NIH HHS R01 NS060648
6 · The paper itself

Abstract

Myosin X (Myo X), also known as MYO10, is an unconventional actin-based motor protein that plays an important role in filopodium formation. Its intra-filopodia movement, an event tightly associated with the function of Myo X, has been extensively studied. However, how the motor activity of Myo X and the direction of its movements are regulated remains largely unknown. In our previous study, we demonstrated that DCC (for 'deleted in colorectal carcinoma') and neogenin (neogenin 1, NEO1 or NGN), a family of immunoglobin-domain-containing transmembrane receptors for netrins, interact with Myo X and that DCC is a cargo of Myo X to be delivered to the neurites of cultured neurons. Here, we provide evidence for DCC and neogenin as regulators of Myo X. DCC promotes movement of Myo X along basal actin filaments and enhances Myo-X-mediated basal filopodium elongation. By contrast, neogenin appears to suppress Myo X movement on the basal side, but increases its movement towards the apical and dorsal side of a cell, promoting dorsal filopodium formation and growth. Further studies have demonstrated that DCC, but not neogenin, enhances integrin-mediated tyrosine phosphorylation of focal adhesion kinase and basal F-actin reorganization, providing a cellular mechanism underlying their distinct effects on Myo X. These results thus demonstrate differential regulatory roles on Myo X activity by its cargo proteins, DCC and neogenin, revealing different cellular functions of DCC and neogenin.

Indexed as

ActinsAnimalsCell CompartmentationCell LineCell MovementDCC ReceptorGreen Fluorescent ProteinsMembrane ProteinsMiceModels, BiologicalMyosinsNeuronsProtein TransportPseudopodiaReceptors, Cell SurfaceRecombinant Fusion ProteinsActinsDcc protein, mouseDCC ReceptorGreen Fluorescent ProteinsMembrane ProteinsMyo10 protein, mouseMyosinsneogeninReceptors, Cell SurfaceRecombinant Fusion ProteinsTumor Suppressor Proteins

Identifiers

PMID22349703
PMCPMC3367835
OpenAlexW2104241818

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.