Author

I. Hamza

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· 1 Microbiology· 1 Pathology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:cell type annotation· 2 Organism:human· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:drug response / drug discovery· 1 Research Focus:host-pathogen & immune response· 1 Organism:mouse· 1 Assay:proteomics· 1

Frequent Co-Authors

X. Yuan· 2 shared A. Bergmann· 1 shared A. R. Reddi· 1 shared A. Ribeiro· 1 shared A. S. Fleischhacker· 1 shared C. Dameron· 1 shared C. M. Moore· 1 shared D. A. Hanna· 1 shared

Activity by Year

2019-2021 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 16 mutual co-author links

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2 shared papersCell Biology

X. Yuan

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Heme oxygenase-2 (HO-2) binds and buffers labile heme, which is largely oxidized, in human embryonic kidney cells

D. A. Hanna, C. M. Moore, L. Liu, X. Yuan, A. S. Fleischhacker, I. Hamza, S. W. Ragsdale, A. R. Reddi

This study shows HO-2 binds and buffers oxidized labile heme in HEK293 cells, regulating heme homeostasis by controlling bioavailability rather than degrading heme under non-stress conditions.

bioRxiv · Jun 6, 2021Cell Biology

Toxoplasma gondii requires its plant-like heme biosynthesis pathway for infection.

A. Bergmann, K. Floyd, M. Key, C. Dameron, K. C. Rees, D. C. Whitehead, I. Hamza, Z. Dou

This study shows Toxoplasma gondii relies on its plant-like heme biosynthesis pathway for infection and demonstrates oxadiazon and its derivatives inhibit growth, suggesting heme biosynthesis as a therapeutic target.

PLOS Pathogens · May 14, 2020Peer-reviewedMicrobiology

Hemozoin produced by mammals confers heme tolerance

R. Pek, X. Yuan, N. Rietzschel, J. Zhang, L. Jackson, E. Nishibori, A. Ribeiro, W. Simmons, J. Jagadeesh, H. Sugimoto, M. Z. Alam, L. Garrett, M. Haldar, M. Ralle, J. Phillips, , I. Hamza

The paper shows that mice lacking HRG1 accumulate excess heme in macrophages, which they tolerate by forming hemozoin, a process previously only observed in blood-feeding parasites.

bioRxiv · May 16, 2019Pathology