Author

Jennifer A. Collins

University of British Columbia

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Genetics· 2 Neuroscience· 1

Signature Assays, Organisms & Methods

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Research Focus:differential expression· 3 Organism:human· 3 Approach:statistical model· 3 Research Focus:gene regulatory network inference· 2 Assay:proteomics· 2 Research Focus:cell type annotation· 1 Assay:DNA methylation· 1 Research Focus:GWAS / association mapping· 1

Frequent Co-Authors

Michael R. HaydeniD· 3 shared Chris KayiD· 2 shared Dale D. O. MartiniD· 2 shared A. Dang· 1 shared A. Kumar· 1 shared Alicia SemakaiD· 1 shared Brett TrostiD· 1 shared Britt I. DrögemölleriD· 1 shared

Activity by Year

2018-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 28 mutual co-author links

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3 shared papersGenetics

Michael R. HaydenORCID

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3 papers

Recent·Most cited

Reduced S-acylation of SQSTM1/p62 in Huntington disease is associated with impaired autophagy

Fatima Abrar, Martyn C. Davies, A. Kumar, A. Dang, Yvonne Nguyen, Jennifer A. Collins, Nicholas S. Caron, J.S. Choudhary, Shaun S. Sanders, Mark O. Collins, Michael R. Hayden, Dale D. O. Martin

The paper shows reduced S-acylation of SQSTM1/p62 in Huntington disease impairs autophagy by blocking autophagic flux and causing empty autophagosomes.

bioRxiv · Oct 11, 2023 · PreprintNeuroscience

Length of uninterrupted CAG repeats, independent of polyglutamine size, results in increased somatic instability and hastened age of onset in Huntington disease

Galen E.B. Wright, Jennifer A. Collins, Chris Kay, Cassandra L. McDonald, Egor Dolzhenko, Qingwen Xia, Kristina Bečanović, Britt I. Drögemöller, Alicia Semaka, Charlotte M. Nguyen, Brett Trost, Fiona Richards, Emilia K. Bijlsma, Ferdinando Squitieri, Colin J. Ross, , Michael R. Hayden

This study identifies a genetic variant that reduces interruption between CAG and CCG repeats in the HTT gene, leading to earlier onset of Huntington disease and increased somatic instability.

The American Journal of Human Genetics · May 16, 2019Peer-reviewedGenetics

A human huntingtin SNP alters post-translational modification and pathogenic proteolysis of the protein causing Huntington disease

Dale D. O. Martin, Chris Kay, Jennifer A. Collins, Yen Thi-Kim Nguyen, R. A. Slama, Michael R. Hayden

The paper identifies a human SNP that modifies post-translational myristoylation of huntingtin, altering its proteolysis and contributing to Huntington disease pathogenesis.

Scientific Reports · May 18, 2018Peer-reviewedGenetics