Evidence map›Paper›PMID 36446770›Full record

ArticleCell death discovery2022

Spatiotemporal control of necroptotic cell death and plasma membrane recruitment using engineered MLKL domains.

Amir Taslimi, Kaiah M Fields, Kristin D Dahl, Qi Liu, Chandra L Tucker

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Optogenetic engineering for precision cancer immunotherapy.Trends in pharmacological sciences · 2025
    Review
  6. Article
  7. Review
  8. Article
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  10. Article
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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.

Amir TaslimiDepartment of Pharmacology, Box 8303, University of Colorado School of Medicine, Aurora, CO, 80045, USA.
Kaiah M FieldsDepartment of Pharmacology, Box 8303, University of Colorado School of Medicine, Aurora, CO, 80045, USA.
Kristin D DahlDepartment of Pharmacology, Box 8303, University of Colorado School of Medicine, Aurora, CO, 80045, USA.
Qi LiuDepartment of Pharmacology, Box 8303, University of Colorado School of Medicine, Aurora, CO, 80045, USA.
Chandra L TuckerDepartment of Pharmacology, Box 8303, University of Colorado School of Medicine, Aurora, CO, 80045, USA. chandra.tucker@cuanschutz.edu.ORCID http://orcid.org/0000-0003-3033-1786
University of Colorado Denver · US

Funding

Uncovering new approaches to manipulate and probe biochemical processes with spatial and temporal precision.R35GM136367 · NIGMS · UNIVERSITY OF COLORADO DENVER · PI Chandra L Tucker · 2020 to 2026
$3.0M
NIGMS NIH HHS R35 GM136367U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) R35GM136367
6 · The paper itself

Abstract

Necroptosis is a form of programmed necrotic cell death in which a signaling cascade induces oligomerization of mixed lineage kinase domain-like (MLKL) protein, leading to plasma membrane rupture. Necroptotic cell death is recognized as important for protection against viral infection and has roles in a variety of diseases, including cancer and diabetes. Despite its relevance to health and disease states, many questions remain about the precise mechanism of necroptotic cell death, cellular factors that can protect cells from necroptosis, and the role of necroptosis in disease models. In this study, we engineered a light-activated version of MLKL that rapidly oligomerizes and is recruited to the plasma membrane in cells exposed to light, inducing rapid cell death. We demonstrate this tool can be controlled spatially and temporally, used in a chemical genetic screen to identify chemicals and pathways that protect cells from MLKL-induced cell death, and used to study signaling responses of non-dying bystander cells. In additional studies, we re-engineered MLKL to block its cell-killing capacity but retain light-mediated membrane recruitment, developing a new single-component optogenetic tool that allows modulation of protein function at the plasma membrane.

Identifiers

PMID36446770
PMCPMC9709077
OpenAlexW4310588812

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.