Evidence map›Paper›PMID 17219248›Full record

ReviewTransgenic research2007

In vivo functions of mitogen-activated protein kinases: conclusions from knock-in and knock-out mice.

Nancy Gerits, Sergiy Kostenko, Ugo Moens

Abstract readReview
PubMed Publisher
In one paragraph

Review in Transgenic research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. p38 MAPK Pathway in the Heart: New Insights in Health and Disease.International journal of molecular sciences · 2020
    Review
  7. ERK: A Key Player in the Pathophysiology of Cardiac Hypertrophy.International journal of molecular sciences · 2019
    Review
  8. Anti-Inflammatory Activity ofInternational journal of molecular sciences · 2018
    Article
  9. Article
  10. Review
  11. Article
  12. Frontiers in pharmacology · 2017
    Review
  13. The JNK Signaling Pathway in Renal Fibrosis.Frontiers in physiology · 2017
    Review
  14. The Role of ERK1/2 in the Development of Diabetic Cardiomyopathy.International journal of molecular sciences · 2016
    Review
  15. Article
  16. Review
  17. Neuroinflammation in Alzheimer's disease.Neuropsychiatric disease and treatment · 2015
    Review
  18. Review
  19. Article
  20. 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

3 authors at 2 institutions in 1 country.

Nancy GeritsDepartment of Microbiology and Virology, Institute of Medical Biology, University of Tromsø, Tromsø, Norway. nancyg@fagmed.uit.no
Sergiy Kostenko
Ugo Moens
UiT The Arctic University of Norway · NOUniversity of Bergen · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multicellular organisms achieve intercellular communication by means of signalling molecules whose effect on the target cell is mediated by signal transduction pathways. Such pathways relay, amplify and integrate signals to elicit appropriate biological responses. Protein kinases form crucial intermediate components of numerous signalling pathways. One group of protein kinases, the mitogen-activated protein kinases (MAP kinases) are kinases involved in signalling pathways that respond primarily to mitogens and stress stimuli. In vitro studies revealed that the MAP kinases are implicated in several cellular processes, including cell division, differentiation, cell survival/apoptosis, gene expression, motility and metabolism. As such, dysfunction of specific MAP kinases is associated with diseases such as cancer and immunological disorders. However, the genuine in vivo functions of many MAP kinases remain elusive. Genetically modified mouse models deficient in a specific MAP kinase or expressing a constitutive active or a dominant negative variant of a particular MAP kinase offer valuable tools for elucidating the biological role of these protein kinases. In this review, we focus on the current status of MAP kinase knock-in and knock-out mouse models and their phenotypes. Moreover, examples of the application of MAP kinase transgenic mice for validating therapeutic properties of specific MAP kinase inhibitors, and for investigating the role of MAP kinase in pathogen-host interactions will be discussed.

Indexed as

MAP Kinase Signaling SystemAnimalsMiceMice, KnockoutMitogen-Activated Protein KinasesModels, AnimalMitogen-Activated Protein Kinases

Identifiers

PMID17219248
OpenAlexW2138005378

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.