Evidence map›Paper›PMID 39921454›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Optogenetically Activatable MLKL as a Standalone Functional Module for Necroptosis and Therapeutic Applications in Antitumoral Immunity.

Da-Hye Jeong, Seokhwi Kim, Han-Hee Park, Kyoung-Jin Woo, Jae-Il Choi, Minji Choi, Jisoo Shin, So Hyun Park, Myung-Wook Seon, Dakeun Lee and 2 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. 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

12 authors.

Da-Hye JeongDepartment of Biochemistry, Ajou University School of Medicine, Suwon, 16499, Republic of Korea.
Seokhwi KimDepartment of Biomedical Science, Graduate School of Ajou University, Suwon, 16499, Republic of Korea.
Han-Hee ParkDepartment of Biochemistry, Ajou University School of Medicine, Suwon, 16499, Republic of Korea.
Kyoung-Jin WooDepartment of Biomedical Science, Graduate School of Ajou University, Suwon, 16499, Republic of Korea.
Jae-Il ChoiDepartment of Pathology, Ajou University School of Medicine, Suwon, 16499, Republic of Korea.
Minji ChoiProgram in Biomedical Science and Engineering, Graduate school, Inha University, Incheon, 22212, Republic of Korea.
Jisoo ShinProgram in Biomedical Science and Engineering, Graduate school, Inha University, Incheon, 22212, Republic of Korea.
So Hyun ParkDepartment of Pathology, Ajou University School of Medicine, Suwon, 16499, Republic of Korea.
Myung-Wook SeonDepartment of Biochemistry, Ajou University School of Medicine, Suwon, 16499, Republic of Korea.
Dakeun LeeDepartment of Biomedical Science, Graduate School of Ajou University, Suwon, 16499, Republic of Korea.
Jong-Ho ChaProgram in Biomedical Science and Engineering, Graduate school, Inha University, Incheon, 22212, Republic of Korea.
You-Sun KimDepartment of Biochemistry, Ajou University School of Medicine, Suwon, 16499, Republic of Korea.ORCID https://orcid.org/0000-0001-6488-3015

Funding

Korea Health Industry Development InstituteKorea Health Technology R&D ProjectMinistry of Health & Welfare, Republic of Korea HR21C1003National Research Foundation of Korea RS-2024-00342075
6 · The paper itself

Abstract

Necroptosis plays a crucial role in the progression of various diseases and has gained substantial attention for its potential to activate antitumor immunity. However, the complex signaling networks that regulate necroptosis have made it challenging to fully understand its mechanisms and translate this knowledge into therapeutic applications. To address these challenges, an optogenetically activatable necroptosis system is developed that allows for precise spatiotemporal control of key necroptosis regulators, bypassing complex upstream signaling processes. The system, specifically featuring optoMLKL, demonstrates that it can rapidly assemble into functional higher-order "hotspots" within cellular membrane compartments, independent of RIPK3-mediated phosphorylation. Moreover, the functional module of optoMLKL significantly enhances innate immune responses by promoting the release of iDAMPs and cDAMPs, which are critical for initiating antitumor immunity. Furthermore, optoMLKL exhibits antitumor effects when activated in patient-derived pancreatic cancer organoids, highlighting its potential for clinical application. These findings will pave the way for innovative cancer therapies by leveraging optogenetic approaches to precisely control and enhance necroptosis.

Indexed as

NecroptosisOptogeneticsPancreatic NeoplasmsProtein KinasesAnimalsCell Line, TumorHumansImmunity, InnateMiceSignal TransductionMLKL protein, humanProtein KinasesimmunotherapyMLKLnecroptosisoptogeneticsorganoidRIPK3

Identifiers

PMID39921454
PMCPMC11967802

What OpenQuestion holds

Textmetadata
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.