Large structural variants in KOLF2.1J are unlikely to compromise neurological disease modeling.

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作者： Mallory,Ryan ^[1] ; Justin A,McDonough ^[1] ; Michael E,Ward ^[2] ; Mark R,Cookson ^[3] ; William C,Skarnes ^[1] ; Florian T,Merkle ^[4]

作者单位： The Jackson Laboratory for Genomic Medicine, Farmington, CT 06032, USA. ^[1] Center for Alzheimer's and Related Dementias (CARD), National Institute on Aging, and National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA. ^[2] Center for Alzheimer's and Related Dementias (CARD), National Institute on Aging, and National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA; Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA. ^[3] Institute of Metabolic Science, and Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0QQ, UK. Electronic address: fm436@cam.ac.uk. ^[4]

DOI 10.1016/j.stem.2024.02.006

PMID 38458177

发布时间 2024-03-22

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Cell stem cell

2024年31卷3期

290-291页

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Large structural variants in KOLF2.1J are unlikely to compromise neurological disease modeling.

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Large structural variants in KOLF2.1J are unlikely to compromise neurological disease modeling.

Cell stem cell

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