Author

Bidisha Bhattacharya

Primary ORCID profile (0009-0001-1294-1516 · 3 papers)Unclaimed ORCID profile · follow to get notified of new preprints

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

Same name, identified by ORCID

Bidisha BhattacharyaiD3 papers · Weizmann Institute of Science

Biology Disciplines

Click to filter author papers

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 2 Research Focus:host-pathogen & immune response· 2 Organism:mouse· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:differential expression· 1 Approach:mechanistic / dynamical model· 1 Assay:metabolomics· 1 Assay:proteomics· 1

Frequent Co-Authors

Alexander Ivanov· 2 shared Alexander Pichugin· 2 shared Bo-Shiun Yan· 2 shared Igor KramnikiD· 2 shared John Connor· 2 shared Lester KobzikiD· 2 shared Robert Berland· 2 shared Yuanwei Gao· 2 shared

Activity by Year

2018-2018 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 45 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

Alexander Ivanov

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

The integrated stress response mediates type I interferon driven necrosis in Mycobacterium tuberculosis granulomas

Bidisha Bhattacharya, Shiqi Xiao, Sujoy Chatterjee, Michael Urbanowski, Alvaro Ordonez, Elizabeth A Ihms, Garima Agrahari, Shichun Lun, Robert Berland, Alexander Pichugin, Yuanwei Gao, John Connor, Alexander Ivanov, Bo-Shiun Yan, Lester Kobzik, , Igor Kramnik

This study identifies the integrated stress response (ISR) as a mediator of necrosis in tuberculosis granulomas, showing that ISR inhibition reduces bacterial burden and necrosis in susceptible mice.

bioRxiv · Dec 19, 2018 · PreprintImmunology

Increased susceptibility to intracellular bacteria and necrotic inflammation driven by a dysregulated macrophage response to TNF

Bidisha Bhattacharya, Sujoy Chattrerjee, Robert Berland, Alexander Pichugin, Yuanwei Gao, John Connor, Alexander Ivanov, Bo-Shiun Yan, Lester Kobzik, Igor Kramnik

The paper identifies a dysregulated macrophage response to TNF in sst1-deficient mice, leading to increased susceptibility to intracellular bacteria and necrotic inflammation.

bioRxiv · Mar 15, 2018 · PreprintImmunology