Evidence map›Paper›PMID 36243838›Full record

ArticleCurrent topics in microbiology and immunology2022

Class I PI3K Biology.

Tihitina Y Aytenfisu, Hannah M Campbell, Mayukh Chakrabarti, L Mario Amzel, Sandra B Gabelli

Abstract read
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In one paragraph

Article in Current topics in microbiology and immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

13 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. The role of PI3K/Akt signaling pathway in chronic kidney disease.International urology and nephrology · 2024
    Review
  12. [Activated phosphoinositide 3-kinase delta syndrome: report of seven cases].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024
    Article
  13. Regulation of PI3K signaling in cancer metabolism and PI3K-targeting therapy.Translational breast cancer research : a journal focusing on translational research in breast cancer · 2024
    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

5 authors at 1 institution in 1 country.

Tihitina Y AytenfisuDepartment of Biophysics and Biophysical Chemistry, The Johns Hopkins School of Medicine, Baltimore, MD, 21205, USA.
Hannah M CampbellDepartment of Biophysics and Biophysical Chemistry, The Johns Hopkins School of Medicine, Baltimore, MD, 21205, USA.
Mayukh ChakrabartiDepartment of Biophysics and Biophysical Chemistry, The Johns Hopkins School of Medicine, Baltimore, MD, 21205, USA.
L Mario AmzelDepartment of Biophysics and Biophysical Chemistry, The Johns Hopkins School of Medicine, Baltimore, MD, 21205, USA.
Sandra B GabelliDepartment of Biophysics and Biophysical Chemistry, The Johns Hopkins School of Medicine, Baltimore, MD, 21205, USA. gabelli@jhmi.edu.
Johns Hopkins University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This chapter is an introduction to phosphoinositide 3-kinases (PI3K), with class I PI3Ks as the central focus. First, the various PI3K isoforms in class I are presented with emphasis on their overall structure, subunits, subunit constitutive domains, domain-domain interactions, and functional relevance. This structural analysis is followed by a comprehensive history of seminal investigations into PI3K activity. Next, we highlight the divergent roles of the isoforms: PI3Kα, PI3Kβ, PI3Kδ, and PI3Kγ. This section details signaling pathways in which these PI3K isoforms are involved, including the key upstream regulators of PI3K activity and some downstream cellular effects. Nodes of the PI3K pathway are also presented. Inhibitors of some isoforms are discussed to give an overview of the basis of some immunotherapies that are being used to target cell signaling. Finally, the chapter ends with a discussion of the dysregulation of PI3Ks in diseases including APDS, asthma, arthritis, and oncogenic mutations.

Indexed as

Phosphatidylinositol 3-KinasesSignal TransductionBiologyPhosphatidylinositolsProtein IsoformsPhosphatidylinositol 3-KinasesPhosphatidylinositolsProtein IsoformsAPDSArthritisAsthmaB-cell signalingChronic inflammationClass I PI3KsOncogenic mutationp101p110βp110γp110δp84Phosphoinositide-3-kinasePI3Kpl10αRas signalingRTK signalingT-cell signaling

Identifiers

PMID36243838
OpenAlexW4306362017

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.