Evidence map›Paper›PMID 34861242›Full record

ArticleBiophysical journal2022

Modeling cell protrusion predicts how myosin II and actin turnover affect adhesion-based signaling.

Ankit Chandra, Mitchell T Butler, James E Bear, Jason M Haugh

Open access · greenAbstract read
In one paragraph

Article in Biophysical journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

12 citing papers in PubMed, 11 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Ankit ChandraDepartment of Chemical and Biomolecular Engineering, North Carolina State University, Raleigh, North Carolina.
Mitchell T ButlerDepartment of Cell Biology and Physiology, UNC Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina.
James E BearDepartment of Cell Biology and Physiology, UNC Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina.
Jason M HaughDepartment of Chemical and Biomolecular Engineering, North Carolina State University, Raleigh, North Carolina. Electronic address: jason_haugh@ncsu.edu.
North Carolina State University · USUniversity of North Carolina at Chapel Hill · US

Funding

Systematic Analysis of the Actin Cytoskeleton and Directed Cell MigrationR35GM130312 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI JAMES E BEAR · 2019 to 2026
$4.8M
Multiscale Modeling of Wound HealingU01EB018816 · NIBIB · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI HAUGH, JASON M. · 2014 to 2021
$4.0M
NIBIB NIH HHS U01 EB018816NIGMS NIH HHS R35 GM130312
6 · The paper itself

Abstract

Orchestration of cell migration is essential for development, tissue regeneration, and the immune response. This dynamic process integrates adhesion, signaling, and cytoskeletal subprocesses across spatial and temporal scales. In mesenchymal cells, adhesion complexes bound to extracellular matrix mediate both biochemical signal transduction and physical interaction with the F-actin cytoskeleton. Here, we present a mathematical model that offers insight into both aspects, considering spatiotemporal dynamics of nascent adhesions, active signaling molecules, mechanical clutching, actin treadmilling, and nonmuscle myosin II contractility. At the core of the model is a positive feedback loop, whereby adhesion-based signaling promotes generation of barbed ends at, and protrusion of, the cell's leading edge, which in turn promotes formation and stabilization of nascent adhesions. The model predicts a switch-like transition and optimality of membrane protrusion, determined by the balance of actin polymerization and retrograde flow, with respect to extracellular matrix density. The model, together with new experimental measurements, explains how protrusion can be modulated by mechanical effects (nonmuscle myosin II contractility and adhesive bond stiffness) and F-actin turnover.

Indexed as

ActinsMyosin Type IIActin CytoskeletonCell Surface ExtensionsSignal TransductionActinsMyosin Type II

Identifiers

PMID34861242
PMCPMC8758409
OpenAlexW3215910002

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.