Evidence map›Paper›PMID 29234486›Full record

ReviewGenes & cancer2017

JNK-signaling: A multiplexing hub in programmed cell death.

Danny N Dhanasekaran, E Premkumar Reddy

Open access · diamondAbstract readReview
In one paragraph

Review in Genes & cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 204 papers.

0numbers the graph read from it
0cells of the map it votes in
204citing papers in PubMed
21.1field-weighted citation impact, top 1% 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

204 citing papers in PubMed, 357 citations in OpenAlex.

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  17. In vitro antitumor effects and apoptosis-related mechanisms of lidocaine in renal cell carcinoma A498 cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  18. World journal of experimental medicine · 2025
    Article
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144 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Danny N DhanasekaranDepartment of Cell Biology, Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma, OK, USA.
E Premkumar ReddyDepartment of Oncological Sciences, and Department of Structural and Chemical Biology, The Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Icahn School of Medicine at Mount Sinai · USUniversity of Oklahoma Health Sciences Center · US

Funding

Targeting Mitotic Kinases Inhibitors for Cancer TherapyR01CA158209 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI REDDY, E PREMKUMAR · 2012 to 2016
$1.7M
Regulation of JNK-signaling molecules by the gep oncogenesR01CA123233 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI DHANASEKARAN, DANNY N. · 2008 to 2013
$1.3M
Identification of Specific Antagonists that Bind Hedgehog and Block its ActivityR15CA159209 · NCI · NORTH CAROLINA CENTRAL UNIVERSITY · PI WILLIAMS, KEVIN PETER · 2011 to 2011
$363k
NCI NIH HHS R01 CA123233NCI NIH HHS R01 CA158209NCI NIH HHS R15 CA159209
6 · The paper itself

Abstract

Jun N-terminal kinases or JNKs have been shown to be involved in a wide array of signaling events underlying tumorigenesis and tumor progression. Through its interaction with a diverse set of signaling proteins and adaptors, JNKs regulate cell proliferation, invasive migration, therapy resistance, and programmed cell death. JNKs have been shown to play a role in apoptotic as well as non-apoptotic programmed cell death mechanisms including those of necroptosis, ferroptosis, pyroptosis, and autophagy. Most of the tumorigenic regulatory functions of JNKs can be related to their ability to module cell death via these programmed cell death mechanisms. JNKs stimulate or inhibit cell death in a context-dependent manner by stimulating the expression of specific genes as well as by modulating the activities of pro- and anti-apoptotic proteins through distinct phosphorylation events. This review summarizes our current understanding of the role of JNK in programmed cell death and its impact on cancer growth, progression, and therapy.

Indexed as

apoptosiscell deathferroptosisJNKnecroptosis

Identifiers

PMID29234486
PMCPMC5724802
OpenAlexW2884510934

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.