Evidence map›Paper›PMID 35328742›Full record

ReviewInternational journal of molecular sciences2022

Crosstalk between p38 MAPK and GR Signaling.

Lisa Zeyen, Ole Morten Seternes, Ingvild Mikkola

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 70 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

3 authors at 1 institution in 1 country.

Lisa ZeyenDepartment of Pharmacy, UiT-The Arctic University of Norway, 9037 Tromsø, Norway.ORCID 0000-0002-9594-6485
Ole Morten SeternesDepartment of Pharmacy, UiT-The Arctic University of Norway, 9037 Tromsø, Norway.
Ingvild MikkolaDepartment of Pharmacy, UiT-The Arctic University of Norway, 9037 Tromsø, Norway.ORCID 0000-0001-6442-7626
UiT The Arctic University of Norway · NO

Funding

Northern Norway Regional Health Authorities HNF1547-20
6 · The paper itself

Abstract

The p38 MAPK is a signaling pathway important for cells to respond to environmental and intracellular stress. Upon activation, the p38 kinase phosphorylates downstream effectors, which control the inflammatory response and coordinate fundamental cellular processes such as proliferation, apoptosis, and differentiation. Dysregulation of this signaling pathway has been linked to inflammatory diseases and cancer. Secretion of glucocorticoids (GCs) is a classical endocrine response to stress. The glucocorticoid receptor (GR) is the primary effector of GCs and plays an important role in the regulation of cell metabolism and immune response by influencing gene expression in response to hormone-dependent activation. Its ligands, the GCs or steroids, in natural or synthetic variation, are used as standard therapy for anti-inflammatory treatment, severe asthma, autoimmune diseases, and several types of cancer. Several years ago, the GR was identified as one of the downstream targets of p38, and, at the same time, it was shown that glucocorticoids could influence p38 signaling. In this review, we discuss the role of the crosstalk between the p38 and GR in the regulation of gene expression in response to steroids and comprehend the importance and potential of this interplay in future clinical applications.

Indexed as

Glucocorticoidsp38 Mitogen-Activated Protein KinasesPhosphorylationReceptors, GlucocorticoidSignal TransductionGlucocorticoidsp38 Mitogen-Activated Protein KinasesReceptors, Glucocorticoidcancercrosslinkdrug discoveryglucocorticoid receptorglucocorticoidsinflammationinhibitorMAPKp38signaling

Identifiers

PMID35328742
PMCPMC8953609
OpenAlexW4220713605

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.