Evidence map›Paper›PMID 41449208›Full record

ArticleExperimental & molecular medicine2025

Optogenetic engineering of BAX to control mitochondrial permeabilization and attenuate apoptosis in cells.

Dain Lee, Hyunjun Bae, Dongwoo Oh, Minseop Kim, Ju-Hee Kim, Jinchul Ahn, Seok-Hyeon Kang, Seo-Hee You, Dong-Hwee Kim, Hyun Jeong Oh and 2 more

Abstract read
In one paragraph

Article in Experimental & molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Immune surveillance interrupted: how cancer exploits trogocytosis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  2. 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.

Dain LeeKU-KIST Graduate School of Converging Science and Technology, Korea University, Seoul, Republic of Korea.
Hyunjun BaeSchool of Mechanical Engineering, Korea University, Seoul, Republic of Korea.
Dongwoo OhKU-KIST Graduate School of Converging Science and Technology, Korea University, Seoul, Republic of Korea.
Minseop KimKU-KIST Graduate School of Converging Science and Technology, Korea University, Seoul, Republic of Korea.
Ju-Hee KimKU-KIST Graduate School of Converging Science and Technology, Korea University, Seoul, Republic of Korea.
Jinchul AhnSchool of Mechanical Engineering, Korea University, Seoul, Republic of Korea.ORCID http://orcid.org/0009-0007-7493-4219
Seok-Hyeon KangSchool of Mechanical Engineering, Korea University, Seoul, Republic of Korea.
Seo-Hee YouSchool of Mechanical Engineering, Korea University, Seoul, Republic of Korea.
Dong-Hwee KimKU-KIST Graduate School of Converging Science and Technology, Korea University, Seoul, Republic of Korea.ORCID http://orcid.org/0000-0003-0625-0660
Hyun Jeong OhSchool of Mechanical Engineering, Korea University, Seoul, Republic of Korea.
Won Do HeoDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea.ORCID http://orcid.org/0000-0001-7541-7319
Seok ChungKU-KIST Graduate School of Converging Science and Technology, Korea University, Seoul, Republic of Korea. sidchung@korea.ac.kr.ORCID http://orcid.org/0000-0002-1735-8338

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although considerable research has focused on enhancing the apoptotic function of BAX for several decades, inhibition of its functionality remains relatively underexplored, despite intensive BAX activation occurring in various neurodegenerative diseases. Here we present a protein engineering approach to modulate BAX integration into the mitochondrial outer membrane, establishing a tunable strategy for antiapoptosis. Utilizing optogenetic methods that employ cryptochrome 2 and its binding partner cryptochrome-interacting basic helix loop helix 1, we achieved precise spatial control over BAX localization, a critical determinant of its function. Our results demonstrate that the engineered BAX variant is effectively incapacitated in its apoptotic function while also modulating endogenous BAX activity to enhance cellular resistance to apoptosis. These findings not only advance our understanding of BAX regulation but also offer promising prospects for the development of therapeutic strategies against apoptosis-related diseases.

Indexed as

Apoptosisbcl-2-Associated X ProteinMitochondriaMitochondrial MembranesOptogeneticsProtein EngineeringCryptochromesHumansPermeabilitybcl-2-Associated X ProteinCryptochromes

Identifiers

PMID41449208
PMCPMC12800262

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.