Author

Sung‐Eun Kim

The University of Texas at AustinORCID 0000-0001-8667-3887Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

Click to filter author papers

Genetics· 2 Biochemistry· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 3 Organism:mouse· 2 Research Focus:cell type annotation· 1 Research Focus:gene regulatory network inference· 1 Organism:human· 1 Assay:proteomics· 1 Approach:statistical model· 1

Frequent Co-Authors

Richard H. FinnelliD· 2 shared Andrew J. KimiD· 1 shared Anna M. BattenhouseiD· 1 shared Bogdan J. WlodarczykiD· 1 shared Gabriella Salazar· 1 shared Hyun Yi Kim· 1 shared Pooja J. Chothani· 1 shared Rehana Shaik· 1 shared

Activity by Year

2023-2026 · peak 1/yr

Co-Author Collaboration Network

9 top collaborators · 12 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

2 shared papersGenetics

Richard H. FinnellORCID

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

BiochemistryPROTEOMICSPeer-reviewedJul 4, 2026

Identification of novel interacting proteins of FUZ and GPR161.

Gabriella Salazar, Anna M. Battenhouse, Andrew J. Kim, Sung‐Eun Kim

This study identifies novel interacting proteins of FUZ and GPR161 using mass spectrometry and GO analysis, revealing their roles in cellular processes and signaling pathways.

DOI 10.1002/pmic.70164

humanproteomics

𝕏 PostBluesky

GeneticsbioRxivPreprintJan 11, 2024

The novel linkage between Fuz and Gpr161 genes regulates sonic hedgehog signaling during mouse embryonic development.

Sung‐Eun Kim, Hyun Yi Kim, Bogdan J. Wlodarczyk, Richard H. Finnell

This study identifies a genetic and biochemical link between Fuz and Gpr161 in regulating sonic hedgehog signaling during mouse embryonic development.

2 citations

mousestatistical model

𝕏 PostBluesky

GeneticsDisease Models & MechanismsPeer-reviewedOct 27, 2023

Pax3 lineage-specific deletion of Gpr161 is associated with spinal neural tube and craniofacial malformations during embryonic development.

Sung‐Eun Kim, Pooja J. Chothani, Rehana Shaik…·Richard H. Finnell

This study shows that deleting Gpr161 in the Pax3 lineage in mice causes spinal and craniofacial defects due to altered Shh and Wnt signaling.

5 citations

mouseexperimental assay

𝕏 PostBluesky