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Fig. 4 | Acta Neuropathologica Communications

Fig. 4

From: Autism-linked mutations of CTTNBP2 reduce social interaction and impair dendritic spine formation via diverse mechanisms

Fig. 4

M120I mutation impairs the N–C terminal interaction of CTTNBP2. a M120I mutation compromises the association of full-length CTTNBP2 with GFP-P-rich fragments. Top: schematics of constructs. Bottom: co-immunoprecipiation (IP) results. Full-length Myc-tagged wild type (Myc-WT) or M120I (Myc-MI) CTTNBP2 proteins were precipitated using Myc tag antibody. Antibody recognizing the C-terminal CTTNBP2 region was used in immunoblotting to recognize all Myc-WT, Myc-MI and GFP-P-rich constructs. GFP vector was used as negative control. b M120I mutation compromised the association of GFP-P-rich fragments with the NCC fragment of CTTNBP2. Top: schematics of constructs. Bottom: co-immunoprecipitation results. Myc-tagged NCC domains (either wild type Myc-NCC or M120I-mutant Myc-NCCMI) were precipitated by Myc tag antibody. Vector only or Mid domain was used as a negative control. Myc and CTTNBP2 antibodies were used for immunoblotting. Arrows point to Myc-tagged constructs, whereas arrowhead indicates GFP-P-rich construct

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