Author

J. Paulo

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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Cell Biology· 2 Cancer Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Assay:proteomics· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:gene regulatory network inference· 1 Organism:human· 1 Assay:metabolomics· 1 Organism:mouse· 1

Frequent Co-Authors

S. Gygi· 2 shared A. Rojaa· 1 shared C. C. Weihl· 1 shared C. S. Clemen· 1 shared C. Thomas· 1 shared D. Duveau· 1 shared G. Q. Fei· 1 shared I. Kline· 1 shared

Activity by Year

2018-2021 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 15 mutual co-author links

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2 shared papersCell Biology

S. Gygi

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

The p97-UBXD8 complex modulates ER-Mitochondria contact sites by modulating membrane lipid saturation and composition

R. Ganji, J. Paulo, Y. Xi, I. Kline, J. Zhu, C. S. Clemen, C. C. Weihl, J. G. Purdy, S. Gygi, M. Raman

This study shows that the p97-UBXD8 complex regulates ER-mitochondria contact sites by modulating membrane lipid saturation and composition, with implications for neurodegenerative diseases.

bioRxiv · Dec 8, 2021 · PreprintCell Biology

O-GlcNAc regulates gene expression by controlling detained intron splicing

Z.-W. Tan, G. Q. Fei, J. Paulo, S. Bellaousov, S. E. S. Martin, D. Duveau, C. Thomas, S. Gygi, P. Boutz, S. Walker

This study shows O-GlcNAc modification regulates detained intron splicing, affecting gene expression and linking nutrient conditions to transcriptional regulation.

bioRxiv · Mar 27, 2020Cell Biology

Identification of endogenous Adenomatous polyposis coli interaction partners and β-catenin-independent targets by proteomics

O. Popow, M. Tatham, J. Paulo, A. Rojaa, N. Loyer, I. P. Newton, J. Januschke, K. Haigis, I. Nathke

The paper identifies APC interaction partners and β-catenin-independent targets using proteomics, revealing MINK1 as a potential substrate of an alternative APC destruction complex.

bioRxiv · Feb 1, 2018Cancer Biology