Evidence map›Paper›PMID 28053086›Full record

ArticleThe Journal of biological chemistry2017

Myosin IIA Heavy Chain Phosphorylation Mediates Adhesion Maturation and Protrusion in Three Dimensions.

Vandana Rai, Dustin G Thomas, Jordan R Beach, Thomas T Egelhoff

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 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
1.4field-weighted citation impact, top 21% 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, 25 citations in OpenAlex.

  1. Article
  2. Nonmuscle myosin 2 turnover in cells is synergistically controlled by the tail and the motor domain.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Non-Muscle Myosin II A: Friend or Foe in Cancer?International journal of molecular sciences · 2024
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. WDR5 modulates cell motility and morphology and controls nuclear changes induced by a 3D environment.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  14. Review
  15. 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

4 authors at 1 institution in 1 country.

Vandana RaiDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195.
Dustin G ThomasDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195.
Jordan R BeachDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195.
Thomas T EgelhoffDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195. Electronic address: tte@case.edu.
Cleveland Clinic Lerner College of Medicine · US

Funding

Myosin Assembly in DictyosteliumR01GM050009 · NIGMS · CLEVELAND CLINIC LERNER COM-CWRU · PI EGELHOFF, THOMAS · 1998 to 2017
$4.7M
NIGMS NIH HHS R01 GM050009
6 · The paper itself

Abstract

Non-muscle myosin II (NMII) is a conserved force-producing cytoskeletal enzyme with important but poorly understood roles in cell migration. To investigate myosin heavy chain (MHC) phosphorylation roles in 3D migration, we expressed GFP-tagged NMIIA wild-type or mutant constructs in cells depleted of endogenous NMIIA protein. We find that individual mutation or double mutation of Ser-1916 or Ser-1943 to alanine potently blocks recruitment of GFP-NM-IIA filaments to leading edge protrusions in 2D, and this in turn blocks maturation of anterior focal adhesions. When placed in 3D collagen gels, cells expressing wild-type GFP MHC-IIA behave like parental cells, displaying robust and active formation and retraction of protrusions. However, cells depleted of NMIIA or cells expressing the mutant GFP MHC-IIA display severe defects in invasion and in stabilizing protrusions in 3D. These studies reveal an NMIIA-specific role in 3D invasion that requires competence for NMIIA phosphorylation at Ser-1916 and Ser-1943. In sum, these results demonstrate a critical and previously unrecognized role for NMIIA phosphorylation in 3D invasion.

Indexed as

Cell AdhesionCell MovementAnimalsCell LineCell Line, TumorChlorocebus aethiopsCOS CellsHumansMiceMyosin Heavy ChainsNonmuscle Myosin Type IIAPhosphorylationMyosin Heavy ChainsNonmuscle Myosin Type IIAcell migrationcytoskeletonextracellular matrixinvasionmyosin

Identifiers

PMID28053086
PMCPMC5336147
OpenAlexW2568565924

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.