Evidence map›Paper›PMID 33002512›Full record

ReviewImmunology letters2020

Regulation of cellular immunity by activating transcription factor 4.

Debasmita Mukherjee, Lena S Bercz, Molly A Torok, Thomas A Mace

Open access · greenAbstract readReview
In one paragraph

Review in Immunology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

30 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Suppression rather than activation of the integrated stress response (GCN2-ATF4) pathway extends lifespan in the fly.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Unfolded protein responses in T cell immunity.Frontiers in immunology · 2024
    Review
  18. Article
  19. Review
  20. Article
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 at 2 institutions in 1 country.

Debasmita MukherjeeThe James Comprehensive Cancer Center, The Ohio State University, Columbus, OH, United States.
Lena S BerczThe James Comprehensive Cancer Center, The Ohio State University, Columbus, OH, United States.
Molly A TorokThe James Comprehensive Cancer Center, The Ohio State University, Columbus, OH, United States.
Thomas A MaceThe James Comprehensive Cancer Center, The Ohio State University, Columbus, OH, United States; Department of Internal Medicine, Division of Gastroenterology, Hepatology and Nutrition, The Ohio State University, Columbus, OH, United States. Electronic address: thomas.mace@osumc.edu.
The Ohio State University · USThe Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute · US

Funding

Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI Tasleem J Padamsee · 1985 to 2026
$132.3M
NCI NIH HHS P30 CA016058
6 · The paper itself

Abstract

Activating transcription factor 4 (ATF4) is a DNA binding transcription factor belonging to the family of basic Leucine zipper proteins. ATF4 can be activated in response to multiple cellular stress signals including endoplasmic reticulum stress in the event of improper protein folding or oxidative stress because of mitochondrial dysfunction as well as hypoxia. There are multiple downstream targets of ATF4 that can coordinate the regulation between survival and apoptosis of a cell based on time and exposure to stress. ATF4, therefore, has a broad range of control that results in the modulation of immune cells of the innate and adaptive responses leading to regulation of the cellular immunity. Studies provide evidence that ATF4 can regulate immune cells such as macrophages, T cells, B cells, NK cells and dendritic cells contributing to progression of disease. Immune cells can be exposed to stressed environment in the event of a pathogen attack, infection, inflammation, or in the tumor microenvironment leading to increased ATF4 activity to regulate these responses. ATF4 can further control differentiation and maturation of different immune cell types becoming a determinant of effective immune regulation. Additionally, ATF4 has been heavily implicated in rendering effector immune cells dysfunctional that are used to target tumorigenesis. Therefore, there is a need to evaluate where the literature stands in understanding the overall role of ATF4 in regulating cellular immunity to identify therapeutic targets and generalized mechanisms for different disease progressions.

Indexed as

Immunity, CellularActivating Transcription Factor 4AnimalsB-LymphocytesDendritic CellsHost-Pathogen InteractionsHumansKiller Cells, NaturalLymphocytesLymphocytes, Tumor-InfiltratingMacrophagesMyeloid-Derived Suppressor CellsNeoplasmsSignal TransductionT-LymphocytesTumor EscapeActivating Transcription Factor 4ATF4 protein, humanATF4Cellular immunityER stressUnfolded protein response

Identifiers

PMID33002512
PMCPMC7688477
OpenAlexW3091765038

What OpenQuestion holds

Textmetadata
LicenceTDM
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.