Author

Claudio Bussi

Nanyang Technological UniversityORCID 0000-0002-9396-9042Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Cell Biology· 1 Developmental Biology· 1

Signature Assays, Organisms & Methods

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Assay:bulk RNA-seq· 2 Organism:human· 2 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Approach:experimental assay· 1 Research Focus:host-pathogen & immune response· 1 Research Focus:metabolism & bioenergetics· 1 Assay:metabolomics· 1

Frequent Co-Authors

Maximiliano Gabriel GutierreziD· 2 shared Ambrosius P. SnijdersiD· 1 shared Callan L BuechsenschuetziD· 1 shared Darryl HaywardiD· 1 shared Dorota Gibbins· 1 shared Elizabeth FisheriD· 1 shared Emmanuel DeauiD· 1 shared Eva Lana‐ElolaiD· 1 shared

Activity by Year

2023-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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2 shared papersCell Biology

Maximiliano Gabriel GutierrezORCID

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2 papers

Recent·Most cited

Cell BiologymBioPeer-reviewedJul 10, 2024

Physiologic media renders human iPSC-derived macrophages permissive for M. tuberculosis by rewiring organelle function and metabolism

Claudio Bussi, Rachel Lai, Natalia Athanasiadi, Maximiliano Gabriel Gutierrez

This study shows that using a human plasma-like medium enhances M. tuberculosis replication in iPSC-derived macrophages by altering lipid metabolism and organelle function.

15 citationstop 4%

humanbulk RNA-seq

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Developmental BiologybioRxivPreprintSep 18, 2023

Congenital heart defects in Down syndrome are caused by increased dosage of DYRK1A

Eva Lana‐Elola, Rifdat Aoidi, Miriam Llorian…·Victor L. J. Tybulewicz

The paper shows increased DYRK1A dosage causes mitochondrial dysfunction and congenital heart defects in Down syndrome, which can be mitigated by a DYRK1A inhibitor.

DOI 10.1101/2023.09.18.558244

humanmouse

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