Evidence map›Paper›PMID 15591622›Full record

ReviewImmunologic research2005

PI3K/AKT signaling and systemic autoimmunity.

Rahul K Patel, Chandra Mohan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Immunologic research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

39 citing papers in PubMed, 89 citations in OpenAlex.

  1. Trial
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  12. Annals of translational medicine · 2022
    Article
  13. Review
  14. Article
  15. Journal of diabetes and metabolic disorders · 2021
    Article
  16. Review
  17. Article
  18. Article
  19. Myeloid disorders after autoimmune disease.Best practice & research. Clinical haematology · 2019
    Review
  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

2 authors at 1 institution in 1 country.

Rahul K PatelDepartment of Rheumatology, UT Southwestern Medical Center at Dallas, Dallas, TX 75390-8884, USA.
Chandra Mohan
The University of Texas Southwestern Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The phosphoinositide 3-kinase (PI3K)/Akt signaling axis plays an important role in cellular proliferation and growth signaling. With respect to the immune system, a growing body of data is helping to elucidate the role of this pathway in lymphocyte development, as well as to show how perturbations that lead to unregulated activation in this pathway may produce systemic autoimmunity or malignancy. Various knockout and transgenic murine models have been described for key mediators of this signaling pathway. Many of these models resulting in the activation of this pathway demonstrate features of systemic autoimmunity, linking this pathway to autoimmune disease. Here, we review recently described murine models that exhibit activated PI3K/Akt signaling and the potential role this pathway in autoimmune disease, and also discuss the therapeutic implications of these findings.

Indexed as

AnimalsAutoimmunityGene ExpressionHumansMicePhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProtein Tyrosine PhosphatasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionTumor Suppressor ProteinsAKT1 protein, humanPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProtein Tyrosine PhosphatasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePten protein, mouseTumor Suppressor Proteins

Identifiers

PMID15591622
OpenAlexW1991240488

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.