Chamberlain Lab

Slide 1

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Intellectual disability (also known as mental retardation) describes a reduced capacity for cognitive processing. There are believed to be a wide range of cellular changes that can result in this condition. These changes can be environmental in origin (e.g. caused by specific diseases, toxins or malnutrition) or can be a result of genetic changes.

Mutations in the zDHHC9 and zDHHC15 genes have been identified as the cause of X-linked intellectual disability in a number of affected individuals. There has so-far been no further analysis examining how zDHHC9 and zDHHC15 dysfunction might cause intellectual disability. However, it is likely that reduced S-acylation of specific zDHHC9/zDHHC15 substrates is important, and proteomic profiling of S-acylation in affected individuals is likely to increase understanding of the molecular basis of this condition. We are currently exploring the links between zDHHC9/zDHHC15 and intellectual disability by investigating the physiological functions, interactions and regulation of these zDHHC enzymes.

Past/Present Sponsors


 Wellcome Trust

Diabetes UK




Palmitoylation is the most prominent type of S-acylation and involves the covalent and reversible attachment of a 16 carbon saturated fatty acid (palmitic acid) to cysteines of target proteins.