Evidence map›Paper›PMID 32540914›Full record

ArticleDisease models & mechanisms2020

A

Anjali Bajpai, Taushif Ahmad Quazi, Hong-Wen Tang, Nishat Manzar, Virender Singh, Ashwani Thakur, Bushra Ateeq, Norbert Perrimon, Pradip Sinha

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Hippo effector, Yorkie, is a tumor suppressor in selectProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. Article
  7. The Importance of mTORC1-Autophagy Axis for Skeletal Muscle Diseases.International journal of molecular sciences · 2022
    Review
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

9 authors at 4 institutions in 2 countries.

Anjali BajpaiBiological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur 208016, India anjalii@iitk.ac.in pradips@iitk.ac.in.ORCID 0000-0002-5645-2466
Taushif Ahmad QuaziBiological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur 208016, India.
Hong-Wen TangDepartment of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Nishat ManzarBiological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur 208016, India.
Virender SinghBiological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur 208016, India.ORCID 0000-0002-6720-8784
Ashwani ThakurBiological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur 208016, India.
Bushra AteeqBiological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur 208016, India.ORCID 0000-0003-4682-9773
Norbert PerrimonDepartment of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Pradip SinhaBiological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur 208016, India anjalii@iitk.ac.in pradips@iitk.ac.in.
Indian Institute of Technology Kanpur · INCase Western Reserve University · USHarvard University · USHoward Hughes Medical Institute · US

Funding

Howard Hughes Medical InstituteWellcome Trust DBT India Alliance IA/E/13/1/501271
6 · The paper itself

Abstract

Peptide therapeutics, unlike small-molecule drugs, display crucial advantages of target specificity and the ability to block large interacting interfaces, such as those of transcription factors. The transcription co-factor of the Hippo pathway, YAP/Yorkie (Yki), has been implicated in many cancers, and is dependent on its interaction with the DNA-binding TEAD/Sd proteins via a large Ω-loop. In addition, the mammalian vestigial-like (VGLL) proteins, specifically their TONDU domain, competitively inhibit YAP-TEAD interaction, resulting in arrest of tumor growth. Here, we show that overexpression of the TONDU peptide or its oral uptake leads to suppression of Yki-driven intestinal stem cell tumors in the adult

Indexed as

Drug DevelopmentAdministration, OralAnimalsAnimals, Genetically ModifiedAntineoplastic AgentsCell ProliferationDisease Models, AnimalDNA-Binding ProteinsDrosophila melanogasterDrosophila ProteinsDrug Screening Assays, AntitumorFemaleGene Expression Regulation, NeoplasticHumansIntestinal NeoplasmsNeoplastic Stem CellsAntineoplastic AgentsDNA-Binding ProteinsDrosophila Proteinsesg protein, DrosophilaNuclear ProteinsPeptide Fragmentssd protein, DrosophilaTrans-ActivatorsTranscription FactorsVGLL1 protein, humanYAP-Signaling ProteinsYki protein, DrosophilaDrosophilaIntegrin signalingIntestinal stem cellsPeptide therapeuticYki

Identifiers

PMID32540914
PMCPMC7390633
OpenAlexW3034391883

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.