Evidence map›Paper›PMID 39724345›Full record

ArticleMethods in molecular biology (Clifton, N.J.)2025

Modulating Optogenetic YAP In Vitro and In Vivo.

Pearlyn Jia Ying Toh

Abstract read
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In one paragraph

Article in Methods in molecular biology (Clifton, N.J.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

1 author.

Pearlyn Jia Ying TohMechanobiology Institute, National University of Singapore, Singapore, Singapore. pearlyn.toh@u.nus.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

YAP is a central regulator of the Hippo-YAP signaling axis, an evolutionarily conserved pathway that modulates organ growth and regeneration. Dysregulation of YAP signaling leads to uncontrolled proliferation, promoting epithelial-to-mesenchymal transition and invasion in cancer metastasis. Exogenous manipulation of YAP activity at the second-to-minute timescale is an important step in studying the signaling pathway. We present an optogenetic system to control the subcellular localization of YAP and therefore its activity as a transcriptional co-activator. We used the LOV2-Jα interacting domains to photocage a nuclear localization signal (NLS) attached to YAP. Under 488 nm light, the Jα helix unfolds and the interaction with LOV2 is disrupted, thereby exposing the NLS and allowing for the entire optogenetic construct to be shuttled into the nucleus. This nuclear translocation is reversible and tuneable and demonstrates functional activity after nuclear localization both in vitro and in vivo.

Indexed as

Cell NucleusNuclear Localization SignalsOptogeneticsTranscription FactorsAdaptor Proteins, Signal TransducingAnimalsHumansMiceSignal TransductionYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingNuclear Localization SignalsTranscription FactorsYAP1 protein, humanYAP-Signaling ProteinsHippo-YAPOptogeneticsSpatiotemporal dynamicsZebrafish

Identifiers

PMID39724345

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.