ReviewCurrent opinion in cell biology2025
Actin cytoskeleton protection by the formin-mediated safety valve.
Review in Current opinion in cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Mechanical forces shape cellular form and function by regulating key cellular processes; however, when dysregulated, they contribute to disease. Excessive forces can be detrimental to cells, damaging cytoskeleton, deforming nuclei, and even rupturing the cell itself. To counteract these effects, cells deploy protective mechanisms that enhance mechanical resilience. Emerging evidence highlights a novel strategy for rapid tension release via force-dependent actin polymerization mediated by formin-family proteins such as Dia1. Acting as a mechanical "safety valve", Dia1 buffers otherwise damaging stress and promotes zyxin-mediated repair, preserving cytoskeletal architecture, safeguarding the nucleus, and maintaining cellular integrity. Loss of Dia1 disrupts signaling cascades that converge on key mechanotransduction processes governing cell fate and disease progression. In this review, we explore recent advances in force-dependent actin polymerization and its role in cytoskeletal protection, nuclear homeostasis, and cellular adaptation to mechanical forces.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.