Evidence map›Paper›PMID 30082911›Full record

ArticleOncogene2019

Induction of store-operated calcium entry (SOCE) suppresses glioblastoma growth by inhibiting the Hippo pathway transcriptional coactivators YAP/TAZ.

Zhijun Liu, Yiju Wei, Lei Zhang, Patricia P Yee, Martin Johnson, Xuexin Zhang, Melissa Gulley, Jennifer M Atkinson, Mohamed Trebak, Hong-Gang Wang and 1 more

Abstract read
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

48 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. A multiple-oscillator mechanism underlies antigen-induced CaThe Journal of biological chemistry · 2023
    Article
  8. Review
  9. CaCellular signalling · 2023
    Review
  10. Neuronal Store-Operated Calcium Channels.Molecular neurobiology · 2023
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Structure and function of the N-terminal extension of the formin INF2.Cellular and molecular life sciences : CMLS · 2022
    Article
  17. Review
  18. Article
  19. Article
  20. 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

11 authors at 2 institutions in 2 countries.

Zhijun LiuDivision of Pediatric Hematology/Oncology, Department of Pediatrics, Penn State Health Hershey Medical Center, Penn State College of Medicine, Hershey, PA, USA.
Yiju WeiDivision of Pediatric Hematology/Oncology, Department of Pediatrics, Penn State Health Hershey Medical Center, Penn State College of Medicine, Hershey, PA, USA.
Lei ZhangDivision of Pediatric Hematology/Oncology, Department of Pediatrics, Penn State Health Hershey Medical Center, Penn State College of Medicine, Hershey, PA, USA.
Patricia P YeeDivision of Pediatric Hematology/Oncology, Department of Pediatrics, Penn State Health Hershey Medical Center, Penn State College of Medicine, Hershey, PA, USA.
Martin JohnsonDepartment of Cellular & Molecular Physiology, Penn State Health Hershey Medical Center, Penn State College of Medicine, Hershey, PA, USA.
Xuexin ZhangDepartment of Cellular & Molecular Physiology, Penn State Health Hershey Medical Center, Penn State College of Medicine, Hershey, PA, USA.
Melissa GulleyDivision of Pediatric Hematology/Oncology, Department of Pediatrics, Penn State Health Hershey Medical Center, Penn State College of Medicine, Hershey, PA, USA.
Jennifer M AtkinsonDivision of Pediatric Hematology/Oncology, Department of Pediatrics, Penn State Health Hershey Medical Center, Penn State College of Medicine, Hershey, PA, USA.
Mohamed TrebakDepartment of Cellular & Molecular Physiology, Penn State Health Hershey Medical Center, Penn State College of Medicine, Hershey, PA, USA.
Hong-Gang WangDivision of Pediatric Hematology/Oncology, Department of Pediatrics, Penn State Health Hershey Medical Center, Penn State College of Medicine, Hershey, PA, USA.
Wei LiDivision of Pediatric Hematology/Oncology, Department of Pediatrics, Penn State Health Hershey Medical Center, Penn State College of Medicine, Hershey, PA, USA. weili@pennstatehealth.psu.edu.ORCID http://orcid.org/0000-0001-5696-4309
Penn State Milton S. Hershey Medical Center · USTongji Hospital · CN

Funding

Penn State Clinical and Translational Science InstituteUL1TR002014 · NCATS · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI KRASCHNEWSKI, JENNIFER L. · 2016 to 2025
$33.7M
Receptor-regulated Ca2+ Entry Pathways in Smooth MuscleR01HL097111 · NHLBI · STATE UNIVERSITY OF NEW YORK AT ALBANY · PI TREBAK, MOHAMED · 2010 to 2019
$3.7M
NRSA Training CoreTL1TR002016 · NCATS · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI THOMAS, GAIL D. · 2016 to 2025
$3.4M
Medical Student Training ProgramT32GM118294 · NIGMS · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI LEVENSON, ROBERT · 2016 to 2021
$1.7M
Leukotriene C4 and STIM/Orai channels in airway smooth muscle remodelingR01HL123364 · NHLBI · STATE UNIVERSITY OF NEW YORK AT ALBANY · PI TREBAK, MOHAMED · 2014 to 2017
$1.5M
The mechanism and function of cell competition in tumorsK22CA190440 · NCI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI LI, WEI · 2015 to 2017
$526k
Genes and miRNAs controlled by ORAI3 in cardiovascular remodelingR21AG050072 · NIA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LEBECHE, DJAMEL, TREBAK, MOHAMED · 2016 to 2017
$471k
American Association for Cancer Research (AACR) 14-20-10-LINCATS NIH HHS TL1 TR002016NCATS NIH HHS UL1 TR002014NCI NIH HHS K22 CA190440NHLBI NIH HHS R01 HL097111NHLBI NIH HHS R01 HL123364NIA NIH HHS R21 AG050072NIGMS NIH HHS T32 GM118294U.S. Department of Health & Human Services | National Institutes of Health (NIH) 5K22CA190440U.S. Department of Health & Human Services | National Institutes of Health (NIH) 5T32GM118294
6 · The paper itself

Abstract

Glioblastomas (GBM) are the most aggressive brain cancers without effective therapeutics. The Hippo pathway transcriptional coactivators YAP/TAZ were implicated as drivers in GBM progression and could be therapeutic targets. Here we found in an unbiased screen of 1650 compounds that amlodipine is able to inhibit survival of GBM cells by suppressing YAP/TAZ activities. Instead of its known function as an L-type calcium channel blocker, we found that amlodipine is able to activate Ca

Indexed as

AcyltransferasesAdaptor Proteins, Signal TransducingAmlodipineAnimalsCalciumCalcium Channel BlockersCalcium SignalingCell Line, TumorEndoplasmic ReticulumEnzyme ActivationFemaleGene Knockdown TechniquesGlioblastomaHippo Signaling PathwayHumansIonomycinAcyltransferasesAdaptor Proteins, Signal TransducingAmlodipineCalciumCalcium Channel BlockersIonomycinNeoplasm ProteinsORAI1 ProteinORAI1 protein, humanPhosphoproteinsProtein Kinase C betaProtein KinasesProtein Serine-Threonine KinasesRecombinant ProteinsRNA, Small InterferingTAFAZZIN protein, humanThapsigarginTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID30082911
PMCPMC6318057
OpenAlexW2887199015

What OpenQuestion holds

Textmetadata
LicenceTDM
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.