Author

K. Friedmann

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

Click to filter author papers

Immunology· 1 Microbiology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

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

Frequent Co-Authors

A. Richter· 2 shared C. Drosten· 2 shared C. Goffinet· 2 shared D. Niemeyer· 2 shared J. Jansen· 2 shared J. Kazmierski· 2 shared A. Balazs· 1 shared A. C. Hocke· 1 shared

Activity by Year

2021-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 42 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

2 shared papersImmunology

A. Richter

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

Non-productive exposure of PBMCs to SARS-CoV-2 induces cell-intrinsic innate immunity responses

J. Kazmierski, K. Friedmann, D. Postmus, C. Fischer, J. Jansen, A. Richter, L. Bosquillon de Jarcy, C. Schüler, M. Sohn, S. Sauer, C. Drosten, A.-E. Saliba, L. Sander, D. Niemeyer, C. Goffinet

The paper shows that non-productive exposure of PBMCs to SARS-CoV-2 triggers JAK/STAT-dependent innate immune responses in monocytes, similar to those seen in mild COVID-19.

bioRxiv · Feb 15, 2022 · PreprintImmunology

Post-entry, spike-dependent replication advantage of B.1.1.7 and B.1.617.2 over B.1 SARS-CoV-2 in an ACE2-deficient human lung cell line

D. Niemeyer, S. Schroeder, K. Friedmann, F. Weege, J. Trimpert, A. Richter, S. Stenzel, J. Jansen, J. Emanuel, J. Kazmierski, F. Pott, L. M. Jeworowski, R. Olmer, M.-C. Jaboreck, B. Tenner, , C. Drosten

The paper shows that B.1.1.7 and B.1.617.2 SARS-CoV-2 variants have a replication advantage over B.1 in ACE2-deficient lung cells, suggesting reliance on alternative cellular factors.

bioRxiv · Oct 20, 2021 · PreprintMicrobiology