Angelman syndrome (AS) is a complex genetic disorder that affects the nervous system. AS affects an estimated 1 in 12,000 to 20,000 individuals [1,2]. Characteristic features of AS include developmental delay or intellectual disability, severe speech impairment, microcephaly, ataxia. Delayed development can be noted by 6 to 12 months of age, and other common signs and symptoms are usually apparent in early childhood.  Although UBE3A is an associated gene with AS, there is a huge gap in our understanding of how lack of  UBE3A leads to AS.  I hypothesize that deregulation of the E6AP-ER complex due to altered UBE3A expression in the brain leads to deregulation of the NPY1R gene and will lead to the development of neurogenetic diseases such as AS. This hypothesis will be experimented in one specific aim: To determine the mechanism by which E6-AP regulates NPY1R in neurons. The overall objective of this aim is to study the potential transcriptional regulation of NPY1R by E6AP in the pathogenesis of AS using neuro2a cell line

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-Alyan Zafar