Huntington’s Disease (HD) is a hereditary neurodegenerative disease; the cause of which is due to a CAG repeat extension in the HTT Gene. This extension is then translated into an elongation of exon 1 which is primarily composed of a disordered PolyQ repeat. Although the cause is known, the mechanism by which this extension affects the function of Huntingtin (HTT), the protein produced by the HTT Gene, has yet to be fully understood. A part of this difficulty is our lack of understanding of the role of normal HTT in our cells. To further our understanding of the role of HTT, we at the SGC have set out to explore the HTT interactome, which will give us a better idea of what specific interactions are modulated in HD. Our first step on this journey was to conduct a literature review alongside a BioID experiment to come up with a list of putative huntingtin interaction partners. One of the hits on the list was GAPDH. This means that we must obtain a pure sample of GAPDH for use in future experiments to further validate the claim that these proteins interact.

Funding Acknowledgment: The SGC is a registered charity (number 1097737) that receives funds from AbbVie, Bayer Pharma AG, Boehringer Ingelheim, Canada Foundation for Innovation, Eshelman Institute for Innovation, Genome Canada through Ontario Genomics Institute [OGI-055], Innovative Medicines Initiative (EU/EFPIA) [ULTRA-DD grant no. 115766], Janssen, Merck KGaA, Darmstadt, Germany, MSD, Novartis Pharma AG,Innovation and Science (MRIS), Pfizer, São Paulo Research Foundation-FAPESP, Takeda, and Wellcome.