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CRISPR/Cas9-induced shank3b mutant zebrafish display autism-like behaviors
2018
Molecular Autism
Human genetic and genomic studies have supported a strong causal role of SHANK3 deficiency in autism spectrum disorder (ASD). However, the molecular mechanism underlying SHANK3 deficiency resulting in ASD is not fully understood. Recently, the zebrafish has become an attractive organism to model ASD because of its high efficiency of genetic manipulation and robust behavioral phenotypes. The orthologous gene to human SHANK3 is duplicated in the zebrafish genome and has two homologs, shank3a and
doi:10.1186/s13229-018-0204-x
pmid:29619162
pmcid:PMC5879542
fatcat:vykqviuq25b2vdga5yzaegrp2u