Author

S. S. Mondal

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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Biochemistry· 1 Cancer Biology· 1 Evolutionary Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:differential expression· 1 Organism:fungi (other)· 1 Research Focus:gene regulatory network inference· 1 Research Focus:host-pathogen & immune response· 1 Organism:mouse· 1

Frequent Co-Authors

A. Carbajal· 1 shared A. Klejman· 1 shared A. Kominek· 1 shared D. F. Jarosz· 1 shared G. Hoser· 1 shared I. Seferynska· 1 shared J. E. Snyder· 1 shared J. Swatler· 1 shared

Activity by Year

2020-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 18 mutual co-author links

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1 shared paperEvolutionary Biology

A. Carbajal

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Author profile →

3 papers

Recent·Most cited

Intercalation of the disulfide bond between the A2 and A4 loop of Cellobiohydrolase (Cel7A) of Aspergillus fumigatus enhances catalytic activity and thermostability

S. Dodda, M. Hossain, S. S. Mondal, S. Das, S. Kahtor (Jain), K. Aikat, S. Mukhopadhyay

This paper introduces disulfide bonds in the A2 and A4 loop of AfCel7A, enhancing its thermostability and catalytic activity compared to the wild type.

bioRxiv · Jul 13, 2023 · PreprintBiochemistry

Targeting Integrated Stress Response by ISRIB combined with imatinib attenuates STAT5 signaling and eradicates therapy-resistant Chronic Myeloid Leukemia cells

W. Dudka, G. Hoser, S. S. Mondal, L. Turos-Korgul, J. Swatler, M. Kusio-Kobiałka, M. Wolczyk, A. Klejman, M. Brewinska-Olchowik, A. Kominek, M. Wiech, M. M. Machnicki, I. Seferynska, T. Stoklosa, K. Piwocka

This study shows that combining ISRIB with imatinib reduces STAT5 signaling and eliminates imatinib-resistant CML cells by altering transcriptomic profiles.

bioRxiv · May 5, 2021 · PreprintCancer Biology

The hunt for ancient prions: Archaeal prion-like domains form amyloids and substitute for yeast prion domains

T. Zajkowski, M. D. Lee, S. S. Mondal, A. Carbajal, R. Dec, P. D. Brennock, R. W. Piast, J. E. Snyder, N. B. Bense, W. Dzwolak, D. F. Jarosz, L. J. Rothschild

This paper identifies prion-like domains in Archaea that form amyloids and transmit non-Mendelian inheritance, suggesting prions existed in the last universal common ancestor.

bioRxiv · Jul 20, 2020 · PreprintEvolutionary Biology