Author

Julian Jude

Primary ORCID profile (0000-0002-9091-9867 · 1 paper)Unclaimed ORCID profile · follow to get notified of new preprints

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Same name, identified by ORCID

Julian JudeiD1 paper · Research Institute of Molecular Pathology

Biology Disciplines

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Biochemistry· 1 Cell Biology· 1

Signature Assays, Organisms & Methods

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Approach:genetic perturbation / CRISPR· 2 Organism:human· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Assay:CRISPR screen· 1 Approach:experimental assay· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

Andreas SchlattliD· 1 shared Catarina P. SantosiD· 1 shared Chiara BernardiniiD· 1 shared Francisco X. RealiD· 1 shared Franziska R. TraubeiD· 1 shared Gordana Wutz· 1 shared Heinrich Kovar· 1 shared Henrik May· 1 shared

Activity by Year

2017-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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1 shared paperCell Biology

Andreas SchlattlORCID

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

CRISPR gene and transcriptome engineering (CRISPRgate) improves loss-of-function genetic screening approaches

Jannis Stadager, Chiara Bernardini, Laura Hartmann, Henrik May, Jessica Wiepcke, Monika Kuban, Zeynab Najafova, Steven A. Johnsen, Stefan Legewie, Franziska R. Traube, Julian Jude, Philipp Rathert

CRISPRgate improves loss-of-function screening by combining CRISPRko and CRISPRi to enhance gene repression and reduce noise in genetic studies.

bioRxiv · May 14, 2024Biochemistry

Hardwired synthetic lethality within the cohesin complex in human cancer cells

Petra van der Lelij, Simone Lieb, Julian Jude, Gordana Wutz, Catarina P. Santos, Katrina Falkenberg, Andreas Schlattl, Jozef Ban, Raphaela Schwentner, Heinrich Kovar, Francisco X. Real, Todd Waldman, Mark A. Pearson, Norbert Kraut, Jan-Michael Peters, , Mark Petronczki

This study identifies a synthetic lethal interaction between STAG1 and STAG2 in cancers with STAG2 mutations, suggesting STAG1 as a therapeutic target.

bioRxiv · Apr 8, 2017 · PreprintCell Biology