Evidence map›Paper›PMID 34764207›Full record

ArticleLife science alliance2022

Integrated stress response restricts macrophage necroptosis.

David E Place, Parimal Samir, Rk Subbarao Malireddi, Thirumala-Devi Kanneganti

Open access · goldAbstract read
In one paragraph

Article in Life science alliance, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

10 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Stress Granules: Novel Regulators of Programmed Cell Death.Mini reviews in medicinal chemistry · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Common virulence factors betweenCurrent research in microbial sciences · 2024
    Review
  9. Review
  10. 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 at 1 institution in 1 country.

David E PlaceDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN, USA.ORCID 0000-0002-1904-4164
Parimal SamirDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN, USA.ORCID 0000-0001-7655-5713
Rk Subbarao MalireddiDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Thirumala-Devi KannegantiDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN, USA Thirumala-Devi.Kanneganti@stjude.org.ORCID 0000-0002-6395-6443
St. Jude Children's Research Hospital · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
Innate immune sensors, inflammasomes, and inflammasome-mediated processes in cancerR35CA253095 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Thirumala-Devi Kanneganti · 2020 to 2026
$7.0M
Role of NLR Inflammasomes in Autoinflammatory Diseases and Host DefenseR01AR056296 · NIAMS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2008 to 2022
$5.9M
The Non-Inflammasome NLRs in Immunity and Host defenseR01AI124346 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Thirumala-Devi Kanneganti · 2016 to 2026
$5.8M
Inflammatory Caspases in Innate Immunity and InflammationR37AI101935 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Thirumala-Devi Kanneganti · 2017 to 2026
$4.9M
Targeting innate immune pathways, and inflammatory cell death in cytokine-mediated diseasesR01AI160179 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2021 to 2025
$4.2M
Inflammatory Caspases in Innate Immunity and InflammationR01AI101935 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2012 to 2016
$2.2M
NCI NIH HHS P30 CA021765NCI NIH HHS R35 CA253095NIAID NIH HHS R01 AI101935NIAID NIH HHS R01 AI124346NIAID NIH HHS R01 AI160179NIAID NIH HHS R37 AI101935NIAMS NIH HHS R01 AR056296
6 · The paper itself

Abstract

The integrated stress response (ISR) regulates cellular homeostasis and cell survival following exposure to stressors. Cell death processes such as apoptosis and pyroptosis are known to be modulated by stress responses, but the role of the ISR in necroptosis is poorly understood. Necroptosis is an inflammatory, lytic form of cell death driven by the RIPK3-MLKL signaling axis. Here, we show that macrophages that have induced the ISR are protected from subsequent necroptosis. Consistent with a reduction in necroptosis, phosphorylation of RIPK1, RIPK3, and MLKL is reduced in macrophages pre-treated with ISR-inducing agents that are challenged with necroptosis-inducing triggers. The stress granule component DDX3X, which is involved in ISR-mediated regulation of pyroptosis, is not required for protecting ISR-treated cells from necroptosis. Disruption of stress granule assembly or knockdown of

Indexed as

NecroptosisStress, PhysiologicalAnimalsCell SurvivalDEAD-box RNA HelicaseseIF-2 KinaseEndoplasmic Reticulum StressFibroblastsGene Knockdown TechniquesMacrophagesMicePhosphorylationReceptor-Interacting Protein Serine-Threonine KinasesStress GranulesToll-Like ReceptorsDdx3x protein, mouseDEAD-box RNA HelicaseseIF-2 KinaseReceptor-Interacting Protein Serine-Threonine KinasesRipk1 protein, mouseRipk3 protein, mouseToll-Like Receptors

Identifiers

PMID34764207
PMCPMC8605341
OpenAlexW3214609147

What OpenQuestion holds

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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 OpenQuestion graph.