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. 2021 Jan 6;18(7):999–1013. doi: 10.1080/15476286.2020.1867797

Table 1.

Dysregulated A-to-I editing associated with neurological or neurodegenerative diseases

Gene Editing site Responsible ADAR1/2 Editing function Associated disease
GRIA2 GluA2 Q→R 2 Change in Ca2+ permeability Amyotrophic lateral sclerosis (ALS) [32,34,39]
Epilepsy [30,45]
Developmental epileptic encephalopathy (DEE) [48–50]
Astrocytoma [55,56]
HT2CR 5-HT2cR A, B, D sites 1 Decrease in 5-HT potency
Reduction in G protein-coupling efficiency
Depression [68,70]
Suicide Schizophrenia [69,70]
Bipolar disorder [70,71]
5-HT2cR C, E sites 1, 2
KCNA1 Kv1.1 I→V 2 Reduction in the deactivation rate Episodic Ataxia Type 1 (EA1) [81], Epilepsy [77]
MIR21 pri-miR-21
8 sites
2 Inhibit Drosha processing Astrocytoma [137]
MIR221 pri-miR-221 − 1, +1, +64 2 Inhibit Drosha processing Astrocytoma [137]
MIR222 pri-miR-222 − 21, +53 2 Inhibit Drosha processing Astrocytoma [137]
MIR376A pri-miR-376a +9 2 Redirection of target recognition of mature miRNA Astrocytoma [138]