Author

Elliot Imler

Biospyder (United States)

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

Biology Disciplines

Click to filter author papers

Biochemistry· 1 Genomics· 1 Neuroscience· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Research Focus:differential expression· 3 Approach:experimental assay· 3 Assay:bulk RNA-seq· 2 Research Focus:cell type annotation· 2 Organism:human· 2 Research Focus:benchmarking· 1 Approach:deep learning· 1 Organism:Drosophila· 1

Frequent Co-Authors

Alex Golkar· 1 shared Alex Rosa CamposiD· 1 shared Amber D. Senese· 1 shared Amit VaishiD· 1 shared Anastasia Velentza· 1 shared Andrew Burritt· 1 shared Animesh Chandra RoyiD· 1 shared Bo ZhouiD· 1 shared

Activity by Year

2019-2025 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

1 shared paperBiochemistry

Alex Golkar

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Discovery of a VHL molecular glue degrader of GEMIN3 by Picowell RNA-seq

Jonathan W. Bushman, Weixian Deng, Kusal T. G. Samarasinghe, Han‐Yuan Liu, Shiqian Li, Amit Vaish, Alex Golkar, Shu Ou, Jinwoo Ahn, Rajesh K. Harijan, Han Han, Tomas Duffy, Elliot Imler, Judy Qiju Wu, Reneé Rawson, , Patrick Ryan Potts

The paper discovers a VHL molecular glue degrader of GEMIN3 using Picowell RNA-seq screening, showing how it targets GEMIN3 for degradation through ternary complex formation.

bioRxiv · Mar 19, 2025 · PreprintBiochemistry

A Drosophila model of neuronal ceroid lipofuscinosis CLN4 reveals a hypermorphic gain of function mechanism

Elliot Imler, Jin Sang Pyon, Selina M. Kindelay, Meaghan Torvund, Yong-quan Zhang, Sreeganga S. Chandra, Konrad E. Zinsmaier

This study develops a Drosophila model of CLN4 NCL, showing that CLN4 mutations cause hypermorphic gain of function through excessive oligomerization and impaired membrane trafficking.

eLife · Oct 30, 2019Peer-reviewedNeuroscience

Extraction-Free Whole Transcriptome Gene Expression Analysis of FFPE Sections and Histology-Directed Subareas of Tissue

Christy L. Trejo, Miloš Babić, Elliot Imler, Migdalia Gonzalez, Sergei I. Bibikov, Peter J. Shepard, Harper C. VanSteenhouse, Joanne M. Yeakley, Bruce E. Seligmann

The paper describes a method to analyze gene expression in FFPE tissues without RNA extraction, showing high correlation with fresh samples and consistent performance across species and tissue areas.

PLoS ONE · Feb 22, 2019Peer-reviewedGenomics