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Tam, Stanley

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Tam, Stanley
Author's Publications: search.filters.isAuthorOfPublication.2379e439-434b-458a-bcb1-7fc68ec5889d

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    Protein interaction network of alternatively spliced isoforms from brain links genetic risk factors for autism
    (Nature Pub. Group, 2014) Corominas, Roser; Yang, Xinping; Lin, Guan Ning; Kang, Shuli; Shen, Yun; Ghamsari, Lila; Broly, Martin; Rodriguez, Maria; Tam, Stanley; Trigg, Shelly A.; Fan, Changyu; Yi, Song; Tasan, Murat; Lemmens, Irma; Kuang, Xingyan; Zhao, Nan; Malhotra, Dheeraj; Michaelson, Jacob J.; Vacic, Vladimir; Calderwood, Michael; Roth, Frederick P.; Tavernier, Jan; Horvath, Steve; Salehi-Ashtiani, Kourosh; Korkin, Dmitry; Sebat, Jonathan; Hill, David; Hao, Tong; Vidal, Marc; Iakoucheva, Lilia M.
    Increased risk for autism spectrum disorders (ASD) is attributed to hundreds of genetic loci. The convergence of ASD variants have been investigated using various approaches, including protein interactions extracted from the published literature. However, these datasets are frequently incomplete, carry biases and are limited to interactions of a single splicing isoform, which may not be expressed in the disease-relevant tissue. Here we introduce a new interactome mapping approach by experimentally identifying interactions between brain-expressed alternatively spliced variants of ASD risk factors. The Autism Spliceform Interaction Network reveals that almost half of the detected interactions and about 30% of the newly identified interacting partners represent contribution from splicing variants, emphasizing the importance of isoform networks. Isoform interactions greatly contribute to establishing direct physical connections between proteins from the de novo autism CNVs. Our findings demonstrate the critical role of spliceform networks for translating genetic knowledge into a better understanding of human diseases.
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    An inter‐species protein–protein interaction network across vast evolutionary distance
    (John Wiley and Sons Inc., 2016) Zhong, Quan; Pevzner, Samuel J; Hao, Tong; Wang, Yang; Mosca, Roberto; Menche, Jörg; Taipale, Mikko; Taşan, Murat; Fan, Changyu; Yang, Xinping; Haley, Patrick; Murray, Ryan R; Mer, Flora; Gebreab, Fana; Tam, Stanley; MacWilliams, Andrew; Dricot, Amélie; Reichert, Patrick; Santhanam, Balaji; Ghamsari, Lila; Calderwood, Michael; Rolland, Thomas; Charloteaux, Benoit; Lindquist, Susan; Barabási, Albert‐László; Hill, David; Aloy, Patrick; Cusick, Michael E; Xia, Yu; Roth, Frederick P; Vidal, Marc
    Abstract In cellular systems, biophysical interactions between macromolecules underlie a complex web of functional interactions. How biophysical and functional networks are coordinated, whether all biophysical interactions correspond to functional interactions, and how such biophysical‐versus‐functional network coordination is shaped by evolutionary forces are all largely unanswered questions. Here, we investigate these questions using an “inter‐interactome” approach. We systematically probed the yeast and human proteomes for interactions between proteins from these two species and functionally characterized the resulting inter‐interactome network. After a billion years of evolutionary divergence, the yeast and human proteomes are still capable of forming a biophysical network with properties that resemble those of intra‐species networks. Although substantially reduced relative to intra‐species networks, the levels of functional overlap in the yeast–human inter‐interactome network uncover significant remnants of co‐functionality widely preserved in the two proteomes beyond human–yeast homologs. Our data support evolutionary selection against biophysical interactions between proteins with little or no co‐functionality. Such non‐functional interactions, however, represent a reservoir from which nascent functional interactions may arise.