Author

A. D. Jayaprakash

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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Cancer Biology· 1 Immunology· 1 Microbiology· 1

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Research Focus:gene regulatory network inference· 2 Organism:human· 2 Approach:statistical model· 2 Assay:bulk RNA-seq· 1 Research Focus:cell-cell communication· 1 Research Focus:clustering· 1

Frequent Co-Authors

R. Sachidanandam· 2 shared S. Hekmaty· 2 shared A. A. Jungbluth· 1 shared A. Bukreyev· 1 shared A. J. Ronk· 1 shared A. Meadows· 1 shared A. N. Prasad· 1 shared C. F. Basler· 1 shared

Activity by Year

2018-2021 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 20 mutual co-author links

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2 shared papersImmunology

R. Sachidanandam

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Author profile →

3 papers

Recent·Most cited

The T cell receptor repertoire reflects the dynamics of the immune response to vaccination

K. Mohammed, A. Meadows, S. Hatem, S. Hekmaty, V. Simon, A. D. Jayaprakash, R. Sachidanandam

This study uses TCR repertoire sequencing to analyze immune responses to vaccines, finding broader T cell responses to COVID-19 than Influenza and TCR as a fingerprint for individual identification.

bioRxiv · Dec 9, 2021 · PreprintImmunology

Marburg and Ebola virus infections elicit a complex, muted inflammatory state in bats

A. D. Jayaprakash, A. J. Ronk, A. N. Prasad, M. F. Covington, K. R. Stein, T. M. Schwarz, S. Hekmaty, K. A. Fenton, T. W. Geisbert, C. F. Basler, A. Bukreyev, R. Sachidanandam

This study investigates how Marburg and Ebola viruses elicit a complex, muted inflammatory response in bats, revealing mechanisms that may explain their non-pathogenicity in these animals.

bioRxiv · Apr 13, 2020Microbiology

YES1 amplification: a mechanism of acquired resistance to EGFR inhibitors identified by transposon mutagenesis and clinical genomics

P.-D. Fan, G. Narzisi, A. D. Jayaprakash, E. Venturini, N. Robine, P. Smibert, S. Germer, H. A. Yu, E. J. Jordan, P. K. Paik, Y. Y. Janjigian, J. E. Chaft, L. Wang, A. A. Jungbluth, S. Middha, , M. Ladanyi

This study identifies YES1 amplification as a novel mechanism of resistance to EGFR inhibitors in lung cancer using transposon mutagenesis and clinical genomic analysis.

bioRxiv · Mar 17, 2018Cancer Biology