Evidence map›Paper›PMID 32752922›Full record

ReviewCell cycle (Georgetown, Tex.)2020

The non-linearity of RAF-MEK signaling in dendritic cells.

Kristina Riegel, Krishnaraj Rajalingam

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2020. 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
0.4field-weighted citation impact, top 40% 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, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. 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

2 authors at 2 institutions in 1 country.

Kristina RiegelCell Biology Unit, University Medical Center Mainz, JGU-Mainz , Mainz, Germany.
Krishnaraj RajalingamCell Biology Unit, University Medical Center Mainz, JGU-Mainz , Mainz, Germany.
Johannes Gutenberg University Mainz · DEUniversity Medical Center of the Johannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kinases form the major part of the druggable genome and their selective inhibition in human cancers has had reasonable clinical success. In contrast to tumorigenesis, the role of kinases in mediating immune responses is poorly understood. However, synergistic therapeutic regimens combining targeted therapy and immune therapy have been found to increase the median survival of tumor patients. In this context, we uncovered that RAF and MEK1/2 kinases, which are the integral parts of the classical MAPK cascade, have unique roles in driving DC differentiation and activation. RAF kinases are stabilized in their protein levels during DC differentiation and are obligatory for normal functioning of DCs. But, the targeting of MEK1/2 kinases with specific inhibitors did not phenocopy the effects observed with RAF inhibitors suggesting that RAF and MEK1/2 kinases may have specific and unique roles in driving immune responses, which deserves further studies to successfully administer these inhibitors in clinics.

Indexed as

Signal TransductionAnimalsAntineoplastic AgentsCell DifferentiationDendritic CellsHumansMAP Kinase Kinase KinasesMolecular Targeted TherapyNeoplasmsPhenotypeProtein Kinase Inhibitorsraf KinasesTumor MicroenvironmentAntineoplastic AgentsMAP Kinase Kinase KinasesProtein Kinase Inhibitorsraf KinasesARAFBRAFCRAFdendritic cells (DCs)InhibitorsMEK1/2 KINASESRAF kinasesT cells

Identifiers

PMID32752922
PMCPMC7513879
OpenAlexW3047016934

What OpenQuestion holds

Textmetadata
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.