Evidence map›Paper›PMID 31396307›Full record

ArticleOxidative medicine and cellular longevity2019

Athanasia Pavlopoulou, Ezgi Karaca, Alma Balestrazzi, Alexandros G Georgakilas

Abstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Molecules (Basel, Switzerland) · 2021
    Article
  5. 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

4 authors.

Athanasia PavlopoulouIzmir International Biomedicine and Genome Institute, Dokuz Eylül University, 35340 Balcova, Izmir, Turkey.ORCID https://orcid.org/0000-0002-0815-3808
Ezgi KaracaIzmir International Biomedicine and Genome Institute, Dokuz Eylül University, 35340 Balcova, Izmir, Turkey.ORCID https://orcid.org/0000-0002-4926-7991
Alma BalestrazziDepartment of Biology and Biotechnology "Lazzaro Spallanzani", University of Pavia, Via Ferrata 1, 27100 Pavia, Italy.ORCID https://orcid.org/0000-0003-2003-4120
Alexandros G GeorgakilasDNA Damage Laboratory, Department of Physics, School of Applied Mathematical and Physical Sciences, National Technical University of Athens (NTUA), Athens, Greece.ORCID https://orcid.org/0000-0002-5971-0010

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The plant innate immune system has two major branches, the pathogen-triggered immunity and the effector-triggered immunity (ETI). The effectors are molecules released by plant attackers to evade host immunity. In addition to the foreign intruders, plants possess endogenous instigators produced in response to general cellular injury termed as damage-associated molecular patterns (DAMPs). In plants, DAMPs or alarmins are released by damaged, stressed, or dying cells following abiotic stress such as radiation, oxidative and drought stresses. In turn, a cascade of downstream signaling events is initiated leading to the upregulation of defense or response-related genes. In the present study, we have investigated more thoroughly the conservation status of the molecular mechanisms implicated in the danger signaling primarily in plants. Towards this direction, we have performed

Indexed as

Signal TransductionAdenosine TriphosphateAlarminsDatabases, FactualMitogen-Activated Protein Kinase 3PhylogenyPlant ProteinsPlantsProtein Interaction MapsProtein Structure, TertiaryAdenosine TriphosphateAlarminsMitogen-Activated Protein Kinase 3Plant Proteins

Identifiers

PMID31396307
PMCPMC6668560

What Socratic 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 Socratic graph.