Simons Searchlight

Maternal modifiers and parent-of-origin bias of the autism-associated 16p11.2 CNV.

A highly penetrant form of childhood apraxia of speech due to deletion of 16p11.2.

Autism spectrum disorder, developmental and psychiatric features in 16p11.2 duplication.

The number of genomic copies at the 16p11.2 locus modulates language, verbal memory, and inhibition.

Auditory evoked M100 response latency is delayed in children with 16p11.2 deletion but not 16p11.2 duplication.

Deletion and duplication of 16p11.2 are associated with opposing effects on visual evoked potential amplitude.

Emergence of a Homo sapiens-specific gene family and chromosome 16p11.2 CNV susceptibility.

16p11.2 deletion and duplication: Characterizing neurologic phenotypes in a large clinically ascertained cohort.

Characterizing cognitive control abilities in children with 16p11.2 deletion using adaptive ‘video game’ technology: A pilot study.

Relationship between M100 auditory evoked response and auditory radiation microstructure in 16p11.2 deletion and duplication carriers.