Genetic manipulation of GSK3B in mice has demonstrated its potential role in social behavior. GSK3B knock-in mice exhibited abnormal social preference, showing no significant preference for novel mouse compared to familiar mouse (Mines et al., 2010). Selective deletion of GSK3B in mouse forebrain pyramidal neurons led to anxiolytic and pro-social effects (Latapy et al., 2012).
Molecular Function
The protein encoded by this gene is a serine-threonine kinase, belonging to the glycogen synthase kinase subfamily. It is involved in energy metabolism, neuronal cell development, and body pattern formation.
External Links
References
Type
Title
Type of Disorder
Associated Disorders
Author, Year
Primary
GSK3 influences social preference and anxiety-related behaviors during social interaction in a mouse model of fragile X syndrome and autism.
Mice with increased activity of GSK3 (21A and 9A knockins) display impaired social memory but have similar anxiety levels and social approach (sociability) as wild type mice.
References
Type
Title
Author, Year
Primary
GSK3 influences social preference and anxiety-related behaviors during social interaction in a mouse model of fragile X syndrome and autism.
Model Type:
Genetic
Model Genotype:
Homozygous
Mutation:
Mice homozygous for GSK3 alpha S21A/S21A/Beta S9A/S9A mutations, these susbtitutions prevent the inhibitory serine phosphorulation of glycogen synthase kinase 3.
Allele Type: Targeted (Knockin)
Strain of Origin: Not Specified
Genetic Background: Not Specified
ES Cell Line: Not Specified
Mutant ES Cell Line: Not Specified
Model Source: Not Specified
Description: Abnormal social preference indicated by no significant preference for novel mouse compared to familiar mouse
Exp Paradigm: Comparison of interaction with familiar s1 mouse and novel s2 mouse
