Evidence map›Paper›PMID 31941025›Full record

ReviewInternational journal of molecular sciences2020

Crosstalk between NLRP12 and JNK during Hepatocellular Carcinoma.

Shahanshah Khan, Hasan Zaki

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 24 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Shahanshah KhanDepartment of Pathology, UT Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0000-0003-3052-932X
Hasan ZakiDepartment of Pathology, UT Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0000-0001-9002-5399
Southwestern Medical Center · US

Funding

Cancer Prevention and Research Institute of Texas (CPRIT) RP160169
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC), a leading cause of cancer-related death, is initiated and promoted by chronic inflammation. Inflammatory mediators are transcriptionally regulated by several inflammatory signaling pathways, including nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK). cJun N-terminal kinase (JNK), a member of the MAPK family, plays a central role in HCC pathogenesis. Pathogen-associated molecular patterns (PAMPs) activate JNK and other MAPK upon recognition by toll-like receptors (TLRs). Apart from TLRs, PAMPs are sensed by several other pattern recognition receptors, including cytosolic NOD-like receptors (NLRs). In a recent study, we demonstrated that the NLR member NLRP12 plays a critical role in suppressing HCC via negative regulation of the JNK pathway. This article briefly reviews the crosstalk between NLRP12 and JNK that occurs during HCC.

Indexed as

MAP Kinase Signaling SystemCarcinoma, HepatocellularHumansIntracellular Signaling Peptides and ProteinsLiver NeoplasmsMAP Kinase Kinase 4Neoplasm ProteinsIntracellular Signaling Peptides and ProteinsMAP Kinase Kinase 4Neoplasm ProteinsNLRP12 protein, humanhepatocellular carcinomainflammationJNKNLRP12

Identifiers

PMID31941025
PMCPMC7013925
OpenAlexW2999415173

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.