ArticleCell death & disease2016
Chronic activation of the D156A point mutant of Channelrhodopsin-2 signals apoptotic cell death: the good and the bad.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Dilating the aging clock with light.Innovation (Cambridge (Mass.)) · 2026Review
- Optogenetics for Investigating and Targeting Hallmark Traits of Cancer.Biomolecules · 2026Review
- Optogenetic Cancer Therapy Using the Light-Driven Outward Proton Pump Rhodopsin Archaerhodopsin-3 (AR3).Journal of the American Chemical Society · 2025Article
- Red-shifted excitation enhances the sensitivity of red genetically encoded CaJournal of biomedical optics · 2025Article
- The Sympathetic Innervation of Adipose Tissues: Regulation, Functions, and Plasticity.Comprehensive Physiology · 2023Article
- Viral Transduction of Human Rod Opsin or Channelrhodopsin Variants to Mouse ON Bipolar Cells Does Not Impact Retinal Anatomy or Cause Measurable Death in the Targeted Cells.International journal of molecular sciences · 2021Article
- Optogenetic control of cancer cell survival in ChR2-transfected HeLa cells.International journal of experimental pathology · 2021Article
- Using a bistable animal opsin for switchable and scalable optogenetic inhibition of neurons.EMBO reports · 2021Article
- Apoptosis of hematopoietic progenitor-derived adipose tissue-resident macrophages contributes to insulin resistance after myocardial infarction.Science translational medicine · 2020Article
- Empowering Retinal Gene Therapy with a Specific Promoter for Human Rod and Cone ON-Bipolar Cells.Molecular therapy. Methods & clinical development · 2020Article
- Toward the Optical Cochlear Implant.Cold Spring Harbor perspectives in medicine · 2019Review
- Optogenetic Peripheral Nerve Immunogenicity.Scientific reports · 2018Article
- Cardiac Optogenetics: 2018.JACC. Clinical electrophysiology · 2018Review
- Synapses in the spotlight with synthetic optogenetics.EMBO reports · 2017Review
- And Then There Was Light: Perspectives of Optogenetics for Deep Brain Stimulation and Neuromodulation.Frontiers in neuroscience · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Channelrhodopsin-2 (ChR2) has become a celebrated research tool and is considered a promising potential therapeutic for neurological disorders. While making its way into the clinic, concerns about the safety of chronic ChR2 activation have emerged; in particular as the high-intensity blue light illumination needed for ChR2 activation may be phototoxic. Here we set out to quantify for the first time the cytotoxic effects of chronic ChR2 activation. We studied the safety of prolonged illumination on ChR2(D156A)-expressing human melanoma cells as cancer cells are notorious for their resistance to killing. Three days of illumination eradicated the entire ChR2(D156A)-expressing cell population through mitochondria-mediated apoptosis, whereas blue light activation of non-expressing control cells did not significantly compromise cell viability. In other words, chronic high-intensity blue light illumination alone is not phototoxic, but prolonged ChR2 activation induces mitochondria-mediated apoptosis. The results are alarming for gain-of-function translational neurological studies but open the possibility to optogenetically manipulate the viability of non-excitable cells, such as cancer cells. In a second set of experiments we therefore evaluated the feasibility to put melanoma cell proliferation and apoptosis under the control of light by transdermally illuminating in vivo melanoma xenografts expressing ChR2(D156A). We show clear proof of principle that light treatment inhibits and even reverses tumor growth, rendering ChR2s potential tools for targeted light-therapy of cancers.
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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.