Evidence map›Paper›PMID 30918126›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

BRCA1/BARD1-dependent ubiquitination of NF2 regulates Hippo-YAP1 signaling.

Sachin Verma, Narayana Yeddula, Yasushi Soda, Quan Zhu, Gerald Pao, James Moresco, Jolene K Diedrich, Audrey Hong, Steve Plouffe, Toshiro Moroishi and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Regulation of placental development and function by ubiquitination.Molecular medicine (Cambridge, Mass.) · 2025
    Review
  3. Article
  4. Role ofCancers · 2024
    Review
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  12. Cancers · 2021
    Review
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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

12 authors at 2 institutions in 1 country.

Sachin VermaLaboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037.
Narayana YeddulaLaboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037.
Yasushi SodaLaboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037.
Quan ZhuLaboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037.
Gerald PaoLaboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037.
James MorescoLaboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037.ORCID 0000-0003-1178-1642
Jolene K DiedrichLaboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037.
Audrey HongDepartment of Pharmacology, University of California, San Diego, La Jolla, CA 92093.
Steve PlouffeDepartment of Pharmacology, University of California, San Diego, La Jolla, CA 92093.
Toshiro MoroishiDepartment of Pharmacology, University of California, San Diego, La Jolla, CA 92093.ORCID 0000-0001-6419-3882
Kun-Liang GuanDepartment of Pharmacology, University of California, San Diego, La Jolla, CA 92093; kuguan@ucsd.edu imohanv1@gmail.com.
Inder M VermaLaboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037; kuguan@ucsd.edu imohanv1@gmail.com.ORCID 0000-0002-4059-075X
Salk Institute for Biological Studies · USUniversity of California San Diego · US

Funding

Viral Vector Core (VVC)P30CA014195 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Ye Zheng · 1985 to 2026
$82.8M
GRADUATE TRAINING IN CELLULAR &MOLECULAR PHARMACOLOGYT32GM007752 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROWN, JOAN HELLER, HANDEL, TRACY M · 1985 to 2023
$13.5M
PROTEIN PHOSPHORYLATION AND GROWTH FACTOR FUNCTIONR01GM051586 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BROWN, JOAN HELLER · 1994 to 2024
$7.9M
The mTOR and Hippo pathway in cell growth and cancerR35CA196878 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUAN, KUN-LIANG · 2015 to 2019
$4.0M
NCI NIH HHS P30 CA014195NCI NIH HHS R35 CA196878NIGMS NIH HHS R01 GM051586NIGMS NIH HHS T32 GM007752
6 · The paper itself

Abstract

Coordination of growth and genomic stability is critical for normal cell physiology. Although the E3 ubiquitin ligase BRCA1 is a key player in maintenance of genomic stability, its role in growth signaling remains elusive. Here, we show that BRCA1 facilitates stabilization of YAP1 protein and turning "off" the Hippo pathway through ubiquitination of NF2. In BRCA1-deficient cells Hippo pathway is "turned On." Phosphorylation of YAP1 is crucial for this signaling process because a YAP1 mutant harboring alanine substitutions (Mt-YAP5SA) in LATS1 kinase recognition sites not only resists degradation but also rescues YAP1 transcriptional activity in BRCA1-deficient cells. Furthermore, an ectopic expression of the active Mt-YAP5SA, but not inactive Mt-YAP6SA, promotes EGF-independent proliferation and tumorigenesis in BRCA1

Indexed as

Signal TransductionUbiquitinationAdaptor Proteins, Signal TransducingAmino Acid SubstitutionBRCA1 ProteinBreast NeoplasmsCell Line, TumorCell ProliferationFemaleHEK293 CellsHippo Signaling PathwayHumansMutation, MissenseNeurofibromin 2PhosphoproteinsProtein Serine-Threonine KinasesAdaptor Proteins, Signal TransducingBARD1 protein, humanBRCA1 ProteinBRCA1 protein, humanLATS1 protein, humanNeurofibromin 2PhosphoproteinsProtein Serine-Threonine KinasesTranscription FactorsTumor Suppressor ProteinsUbiquitin-Protein LigasesYAP1 protein, humanYAP-Signaling ProteinsBRCA1cancerHippoNF2ubiquitination

Identifiers

PMID30918126
PMCPMC6462108
OpenAlexW2924520368

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.