Author

S. B. van Engelenburg

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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Microbiology· 2 Cell Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Research Focus:host-pathogen & immune response· 2 Organism:human· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:database / resource· 1 Organism:Drosophila· 1 Assay:electronic health records· 1

Frequent Co-Authors

H. K. Hoffman· 3 shared E. O. Freed· 2 shared A. Müller· 1 shared A. T. Ritter· 1 shared A. V. Weigel· 1 shared C. S. Xu· 1 shared D. Bennett· 1 shared G. Shtengel· 1 shared

Activity by Year

2020-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 31 mutual co-author links

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3 shared papersMicrobiology

H. K. Hoffman

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

MicrobiologybioRxivPreprintJun 3, 2022

Rab11-FIP1C is dispensable for HIV-1 replication in primary CD4+ T cells but its role is cell-type-dependent in immortalized human T-cell lines

E. O. Freed, M. V. de Cespedes, H. K. Hoffman…·S. B. van Engelenburg

This study shows FIP1C is not essential for HIV-1 replication in primary CD4+ T cells but has cell-type-dependent effects in T-cell lines.

DOI 10.1101/2022.06.03.494784

humanbulk RNA-seq

Cell BiologyNaturePeer-reviewedOct 6, 2021

An open-access volume electron microscopy atlas of whole cells and tissues

C. S. Xu, S. Pang, G. Shtengel…·H. Hess

The paper presents a 3D electron microscopy atlas of whole cells and tissues with high resolution and large volume, enabling new biological insights.

DOI 10.1038/s41586-021-03992-4

mouseDrosophila

MicrobiologyJournal of VirologyPeer-reviewedNov 9, 2020

Elucidating the basis for permissivity of the MT-4 T-cell line to replication of an HIV-1 mutant lacking the gp41 cytoplasmic tail

M. V. Fernandez, H. K. Hoffman, N. Pezeshkian…·E. O. Freed

This study investigates why MT-4 T-cells allow HIV-1 replication despite lacking the gp41 cytoplasmic tail, finding faster viral production, higher surface Env, and increased cell-to-cell transmission contribute to this permissivity.

DOI 10.1128/jvi.01334-20

humanproteomics