Author

Jonathan Crain

Cold Spring Harbor Laboratory

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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Developmental Biology· 1 Genomics· 1 Systems Biology· 1

Signature Assays, Organisms & Methods

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Approach:statistical model· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Approach:experimental assay· 1 Organism:human· 1 Organism:mouse· 1 Assay:proteomics· 1

Frequent Co-Authors

Gholson J. LyoniD· 2 shared Max Johannes Dörfel· 2 shared Ahmed Ismail· 1 shared Alison J. SeboldiD· 1 shared Andrew Garcia· 1 shared Catherine E. KeeganiD· 1 shared Cheolju LeeiD· 1 shared David Bolton· 1 shared

Activity by Year

2016-2021 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 30 mutual co-author links

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2 shared papersDevelopmental Biology

Gholson J. LyonORCID

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Author profile →

3 papers

Recent·Most cited

Naa12 compensates for Naa10 in mice in the amino-terminal acetylation pathway

Hyae Yon Kweon, Mi-Ni Lee, Max Johannes Dörfel, Seungwoon Seo, Leah Gottlieb, Thomas Papazyan, Nina McTiernan, Rasmus Ree, David Bolton, Andrew Garcia, Michael J. Flory, Jonathan Crain, Alison J. Sebold, Scott K. Lyons, Ahmed Ismail, , Gholson J. Lyon

The paper identifies Naa12 as a compensatory N-terminal acetyltransferase that rescues Naa10 deficiency in mice, revealing its role in amino-terminal acetylation.

eLife · Aug 6, 2021Peer-reviewedDevelopmental Biology

Not by systems alone: replicability assessment of disease expression signals

Sara Ballouz, Max Johannes Dörfel, Megan Crow, Jonathan Crain, Laurence Olivier Faivre, Catherine E. Keegan, Sophia Kitsiou‐Tzeli, Maria Tzetis, Gholson J. Lyon, Jesse A Gillis

The paper assesses the replicability of disease expression signals across pedigrees and identifies genes missed by systems methods.

bioRxiv · Dec 26, 2018 · PreprintSystems Biology

Proteomic and genomic characterization of a yeast model for Ogden syndrome

Max Doerfel, Han Fang, Jonathan Crain, Michael E Klingener, Jake Weiser, Gholson J Lyon

The paper characterizes a yeast model of Ogden syndrome, showing the S37P mutation disrupts Naa10 function and affects cellular processes like chaperone activity and gene expression.

bioRxiv · Jul 12, 2016Genomics