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Researchers have boosted the efficiency of prime editing, a highly versatile CRISPR-based gene editing technology, and used the improved system to correct disease mutations in cells.

Converting a pathogenic hemoglobin gene to a benign variant enables healthy blood cell production in an animal model of sickle cell disease.

By engineering proteins called proteases to find new targets with high selectivity, researchers mark a critical advance toward potential new treatments for a wide range of conditions

Correcting the mutation that causes progeria with base editing leads to strong symptom reduction and longer lifespan in an animal model

An engineered bacterial toxin is a key part of a gene editor that can make single-base changes in human mitochondria.

BE-Hive can tell which base editor performs best to repair thousands of disease-causing mutations

By showing they could repair a single recessive mutation behind a form of hearing loss, researchers open the door to using base editing to address a broader range of conditions

A new adenine base editor expands the range of genetic sites that can be edited in human cells, with speed and efficiency far surpassing the original editor.

New CRISPR base editors make fewer off-target edits and can access more locations on the genome than earlier versions.

“Prime editing” combines two key proteins and a new RNA to make targeted insertions, deletions, and all possible single-letter changes in the DNA of human cells