清脆的
基因组编辑
生物
医学
计算生物学
生物信息学
神经科学
药理学
遗传学
基因
作者
Benjamin Ng,Maria Kaukonen,Michelle E. McClements,Hoda Shamsnajafabadi,Robert E. MacLaren,Jasmina Cehajic‐Kapetanovic
标识
DOI:10.1016/j.preteyeres.2024.101289
摘要
Conventional gene therapy involving supplementation only treats loss-of-function diseases and is limited by viral packaging sizes, precluding therapy of large genes. The discovery of CRISPR/Cas has led to a paradigm shift in the field of genetic therapy, with the promise of precise gene editing, thus broadening the range of diseases that can be treated. The initial uses of CRISPR/Cas have focused mainly on gene editing or silencing of abnormal variants via utilising Cas endonuclease to trigger the target cell endogenous non-homologous end joining. Subsequently, the technology has evolved to modify the Cas enzyme and even its guide RNA, leading to more efficient editing tools in the form of base and prime editing. Further advancements of this CRISPR/Cas technology itself have expanded its functional repertoire from targeted editing to programmable transactivation, shifting the therapeutic focus to precise endogenous gene activation or upregulation with the potential for epigenetic modifications. In vivo experiments using this platform have demonstrated the potential of CRISPR-activators (CRISPRa) to treat various loss-of-function diseases, as well as in regenerative medicine, highlighting their versatility to overcome limitations associated with conventional strategies. This review summarises the molecular mechanisms of CRISPRa platforms, the current applications of this technology in vivo , and discusses potential solutions to translational hurdles for this therapy, with a focus on ophthalmic diseases. • Conventional exogeneous gene replacement cannot be used to treat inherited ocular conditions caused by large genes. • CRISPR/Cas technologies expand the treatment repertoire via specifically editing or knocking out specific mutations. • CRISPR activation can supplement haploinsufficient conditions and activate paralogs of large mutant genes.
科研通智能强力驱动
Strongly Powered by AbleSci AI