Evidence map›Paper›PMID 37934809›Full record

ArticleScience signaling2023

A conserved mechanism for JNK-mediated loss of Notch function in advanced prostate cancer.

Cheng-Wei Wang, Marie Clémot, Takao Hashimoto, Johnny A Diaz, Lauren M Goins, Andrew S Goldstein, Raghavendra Nagaraj, Utpal Banerjee

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Science signaling, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 32% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Article
  3. Notch Signaling in Drosophila Tumor Models.Advances in experimental medicine and biology · 2025
    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

8 authors at 1 institution in 1 country.

Cheng-Wei WangDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA, USA.ORCID 0009-0003-9962-949X
Marie ClémotDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA, USA.ORCID 0000-0003-4992-1524
Takao HashimotoDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA, USA.ORCID 0000-0002-7205-0897
Johnny A DiazDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA, USA.
Lauren M GoinsDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA, USA.
Andrew S GoldsteinDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA, USA.ORCID 0000-0003-0434-9149
Raghavendra NagarajDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA, USA.ORCID 0009-0005-8819-0092
Utpal BanerjeeDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA, USA.ORCID 0000-0001-6247-0284
University of California, Los Angeles · US

Funding

TUMOR CELL SURFACES AND CHROMOSOMEST32CA009056 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Gay M Crooks, David A. Nathanson · 1985 to 2026
$10.5M
Genomic and Genetic Dissection of Hematopoietic Development in DrosophilaR01HL067395 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SIEKHAUS, DARIA E · 2001 to 2025
$9.0M
Metabolic and signaling control of tumorformation in drosophilaR01CA217608 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BANERJEE, UTPAL · 2017 to 2021
$1.8M
Mechanisms of Asymmetric Cell Division in Developmental HematopoiesisK01DK132488 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Lauren Monica Goins · 2022 to 2026
$845k
NCI NIH HHS R01 CA217608NCI NIH HHS T32 CA009056NHLBI NIH HHS R01 HL067395NIDDK NIH HHS K01 DK132488
6 · The paper itself

Abstract

Dysregulated Notch signaling is a common feature of cancer; however, its effects on tumor initiation and progression are highly variable, with Notch having either oncogenic or tumor-suppressive functions in various cancers. To better understand the mechanisms that regulate Notch function in cancer, we studied Notch signaling in a

Indexed as

Drosophila ProteinsProstatic NeoplasmsAnimalsDrosophilaHumansMaleReceptors, NotchSignal TransductionDrosophila ProteinsReceptors, Notch

Identifiers

PMID37934809
PMCPMC10802904
OpenAlexW4388451863

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.