Evidence map›Paper›PMID 26542704›Full record

ReviewDisease models & mechanisms2015

Non-muscle myosin II in disease: mechanisms and therapeutic opportunities.

Karen A Newell-Litwa, Rick Horwitz, Marcelo L Lamers

Abstract readReview
In one paragraph

Review in Disease models & mechanisms, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

107 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  6. Non-transport functions of motor proteins in corticogenesis.Frontiers in cell and developmental biology · 2026
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47 more citing papers are in PubMed but not listed here.

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

3 authors.

Karen A Newell-LitwaDepartment of Cell Biology, University of Virginia, Charlottesville, VA 22908, USA kal8m@virginia.edu.
Rick HorwitzDepartment of Cell Biology, University of Virginia, Charlottesville, VA 22908, USA.
Marcelo L LamersDepartment of Morphological Sciences, Institute of Basic Health Science, Federal University of Rio Grande do Sul, Porto Alegre, Rio Grande do Sul 90610-010, Brazil.

Funding

DETERMINANTS OF MYOGENIC MEMBRANE PHENOMENAR01GM023244 · NIGMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI HORWITZ, ALAN F. "RICK" · 1985 to 2014
$6.7M
DETERMINANTS OF MYOGENIC MEMBRANE PHENOMENAR37GM023244 · NIGMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI HORWITZ, ALAN F · 1992 to 2002
$1.1M
NIGMS NIH HHS GM23244NIGMS NIH HHS R01 GM023244NIGMS NIH HHS R37 GM023244
6 · The paper itself

Abstract

The actin motor protein non-muscle myosin II (NMII) acts as a master regulator of cell morphology, with a role in several essential cellular processes, including cell migration and post-synaptic dendritic spine plasticity in neurons. NMII also generates forces that alter biochemical signaling, by driving changes in interactions between actin-associated proteins that can ultimately regulate gene transcription. In addition to its roles in normal cellular physiology, NMII has recently emerged as a critical regulator of diverse, genetically complex diseases, including neuronal disorders, cancers and vascular disease. In the context of these disorders, NMII regulatory pathways can be directly mutated or indirectly altered by disease-causing mutations. NMII regulatory pathway genes are also increasingly found in disease-associated copy-number variants, particularly in neuronal disorders such as autism and schizophrenia. Furthermore, manipulation of NMII-mediated contractility regulates stem cell pluripotency and differentiation, thus highlighting the key role of NMII-based pharmaceuticals in the clinical success of stem cell therapies. In this Review, we discuss the emerging role of NMII activity and its regulation by kinases and microRNAs in the pathogenesis and prognosis of a diverse range of diseases, including neuronal disorders, cancer and vascular disease. We also address promising clinical applications and limitations of NMII-based inhibitors in the treatment of these diseases and the development of stem-cell-based therapies.

Indexed as

DiseaseAnimalsCell- and Tissue-Based TherapyHumansMolecular Targeted TherapyMyosin Type IIMyosin Type IIMigrationMyosinNMIIStem cellSynapse

Identifiers

PMID26542704
PMCPMC4728321

What OpenQuestion holds

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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.