ArticleCell2016
Naturally Occurring Off-Switches for CRISPR-Cas9.
Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 231 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
231 citing papers in PubMed, 1 synthesis or guideline pooled it, 411 citations in OpenAlex.
- CRISPR-Cas systems as next-generation antimicrobials: a systemic review of mechanisms, delivery strategies, and translational challenges.Frontiers in microbiology · 2026Pooled it
- Strategies and mechanisms of precision genome engineering: From gene editing to genome writing.iMetaOmics · 2026Review
- Potential role of a CRISPR-Cas-activated toxin-antitoxin system in bacterial immunity.Nature communications · 2026Article
- SauCas9-based cell cycle-dependent genome editing via AAV delivery.Molecular therapy. Advances · 2026Article
- Programmable spatiotemporal control of CRISPR-Cas12a: Engineering precision for next-generation gene editing and diagnostics.Synthetic and systems biotechnology · 2026Review
- Investigating the molecular mechanisms underlying the anti-CRISPR function of AcrIIA13b protein.The FEBS journal · 2026Article
- CRISPR-anti-CRISPR dynamics: evolutionary, ecological and biotechnological perspectives.Archives of microbiology · 2026Review
- AcrIIA7 hijacks tracrRNA to block CRISPR-Cas system.Nature communications · 2026Article
- A Computational Model for Nme1Cas9 HNH Activation Driven by Dynamic Interface Engineering at Residues S593 and W596.Biomolecules · 2026Article
- Semantic design: Programming functional genes from genomic context.Cell genomics · 2026Article
- An anti-CRISPR targets the sgRNA to block Cas9 and guides the design of enhanced genome editors.Nature structural & molecular biology · 2026Article
- Bio-orthogonal chemistry-based strategy to Turn-OFF CRISPR-Cas9 activity in solution and live cells.NAR molecular medicine · 2026Article
- Phage-plasmid-like elements are found throughout diverse environments and encode niche-specific functional traits.PloS one · 2026Article
- Article
- Regulation of anti-CRISPR operons by structurally distinct families of Aca proteins.Communications biology · 2025Article
- Photocontrolled dissociation and toehold-mediated strand displacement-based synergistic regulation of CRISPR-Cas12a.Nucleic acids research · 2025Article
- Controlling CRISPR-Cas9 genome editing in human cells using a molecular glue degrader.Molecular therapy. Nucleic acids · 2025Article
- Protective antigen-mediated delivery of an anti-CRISPR protein for precision genome editing.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Identification of regulatory sequences in Aca11 and Aca13 for detection of anti-CRISPR and protein-protein interaction.Nucleic acids research · 2025Article
- Gene regulation technologies for gene and cell therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
171 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
CRISPR-Cas9 technology would be enhanced by the ability to inhibit Cas9 function spatially, temporally, or conditionally. Previously, we discovered small proteins encoded by bacteriophages that inhibit the CRISPR-Cas systems of their host bacteria. These "anti-CRISPRs" were specific to type I CRISPR-Cas systems that do not employ the Cas9 protein. We posited that nature would also yield Cas9 inhibitors in response to the evolutionary arms race between bacteriophages and their hosts. Here, we report the discovery of three distinct families of anti-CRISPRs that specifically inhibit the CRISPR-Cas9 system of Neisseria meningitidis. We show that these proteins bind directly to N. meningitidis Cas9 (NmeCas9) and can be used as potent inhibitors of genome editing by this system in human cells. These anti-CRISPR proteins now enable "off-switches" for CRISPR-Cas9 activity and provide a genetically encodable means to inhibit CRISPR-Cas9 genome editing in eukaryotes. VIDEO ABSTRACT.
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What OpenQuestion holds
Registered trials
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.