Modernising autism spectrum disorder model engineering and treatment via CRISPR-Cas9: A gene reprogramming approach

Table 2 Summary of clustered regularly interspaced palindromic repeats-associated protein 9 edited therapeutic targets of autism spectrum disorder

Ref.	In vitro/invivo	Gene mutation/editing method	Observed alterations
[80-82]	BTBR T + tf/J (BTBR), Fmr1 knockout, C57BL/6 mice	mGluR5	Rescued the exaggerated repetitive behaviours in mice caused by fragile X syndrome
[83]	HEK293 cell and Human iPSC (BCRT cell line)	MECP2	Reversal of ASD-associated Rett syndrome-like symptoms
[84]	RX41X iPSC and NOD/SCID female mice	SHANK2	Positive impact on nerve cells was reported like an increase in synapse number, dendritic complexity and length
[85]	C57BL/6 mice, Ube3am-/p+ mice and Ube3am-/pYFP mice on the C57Bl/6	Antisense transcript of UBE3A	Rescued the anatomical and behavioural phenotypes in a mouse model of Angelman syndrome
[86]	HEK293FT cells	FMR1	Fragile X syndrome improved by knocking out the CGG
[89]	Mef2c L35P knock-in mouse	MEF2C	Reversal of autistic-like behaviour

ASD: Autism spectrum disorder; CGG: Cytosine-guanine-guanine; FMR1/Fmr1: Fragile X messenger ribonucleoprotein 1; iPSC: Induced pluripotent stem cell; MECP2: Methyl CpG binding protein 2; MEF2C: Myocyte-specific enhancer factor 2C; mGluR5: Metabotropic glutamate receptor subtype 5; SHANK2: SH3- and multiple ankyrin repeats protein 2.