Evidence map›Paper›PMID 31996378›Full record

ArticleThe Journal of biological chemistry2020

Furry protein suppresses nuclear localization of yes-associated protein (YAP) by activating NDR kinase and binding to YAP.

Kazuki Irie, Tomoaki Nagai, Kensaku Mizuno

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  3. Homer condensates orchestrate YAP-Wnt signaling crosstalk downstream of the Crumbs polarity complex.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

3 authors at 1 institution in 1 country.

Kazuki IrieDepartment of Molecular and Chemical Life Sciences, Graduate School of Life Sciences, Tohoku University, Aobayama, Sendai, Miyagi 980-8578, Japan.
Tomoaki NagaiDepartment of Molecular and Chemical Life Sciences, Graduate School of Life Sciences, Tohoku University, Aobayama, Sendai, Miyagi 980-8578, Japan.
Kensaku MizunoDepartment of Molecular and Chemical Life Sciences, Graduate School of Life Sciences, Tohoku University, Aobayama, Sendai, Miyagi 980-8578, Japan; Institute of Liberal Arts and Sciences, Tohoku University, Kawauchi, Sendai, Miyagi 980-8576, Japan. Electronic address: kmizuno@biology.tohoku.ac.jp.
Tohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Hippo signaling pathway suppresses cell proliferation and tumorigenesis. In the canonical Hippo pathway, large tumor suppressor kinases 1/2 (LATS1/2) phosphorylate the transcriptional coactivator yes-associated protein (YAP) and thereby suppress its nuclear localization and co-transcriptional activity. Nuclear Dbf2-related kinases 1/2 (NDR1/2), which are closely related to LATS1/2, also phosphorylate and inactivate YAP by suppressing its nuclear localization. Furry (FRY) is a cytoplasmic protein that associates with NDR1/2 and activates them, but its role in the nuclear/cytoplasmic localization of YAP remains unknown. Here, we constructed FRY-knockout cell lines to examine the role of FRY in YAP's cytoplasmic localization. FRY depletion markedly increased YAP nuclear localization and decreased NDR1/2 kinase activity and YAP phosphorylation levels, but did not affect LATS1/2 kinase activity. This indicated that FRY suppresses YAP's nuclear localization by promoting its phosphorylation via NDR1/2 activation. NDR1/2 depletion also promoted YAP nuclear localization, but depletion of both FRY and NDR1/2 increased the number of cells with YAP nuclear localization more strongly than did depletion of NDR1/2 alone, suggesting that FRY suppresses YAP nuclear localization by a mechanism in addition to NDR1/2 activation. Co-precipitation assays revealed that Fry uses its N-terminal 1-2400-amino-acid-long region to bind to YAP. Expression of full-length FRY or its 1-2400 N-terminal fragment restored YAP cytoplasmic localization in FRY-knockout cells. Taken together, these results suggest that FRY plays a crucial role in YAP cytoplasmic retention by promoting YAP phosphorylation via NDR1/2 kinase activation and by binding to YAP, leading to its cytoplasmic sequestration.

Indexed as

Adaptor Proteins, Signal TransducingCell Cycle ProteinsCell NucleusCytoplasmGene EditingHEK293 CellsHumansPhosphorylationProtein BindingProtein Serine-Threonine KinasesRNA InterferenceRNA, Small InterferingSignal TransductionTranscription FactorsYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingCell Cycle ProteinsFRY protein, humanLATS1 protein, humanProtein Serine-Threonine KinasesRNA, Small InterferingSTK38L protein, humanSTK38 protein, humanTranscription FactorsYAP1 protein, humanYAP-Signaling Proteinscancercell signalingFurry (FRY)gene knockoutHippo pathwaylarge tumor suppressor kinase (LATS)NDR (nuclear Dbf2-related) kinasephosphorylationprotein kinaseyes-associated protein (YAP)

Identifiers

PMID31996378
PMCPMC7062186
OpenAlexW3003446887

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.