Author

A. R. Subbalakshmi

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

Cancer Biology· 5

Signature Assays, Organisms & Methods

Click to filter · or open tag

Assay:bulk RNA-seq· 4 Organism:human· 4 Research Focus:cell type annotation· 3 Approach:statistical model· 3 Research Focus:gene regulatory network inference· 2 Research Focus:chromatin & epigenetic regulation· 1 Approach:comparative / phylogenetic analysis· 1 Research Focus:differential expression· 1

Frequent Co-Authors

M. K. Jolly· 5 shared S. Sahoo· 3 shared I. McMullen· 2 shared J. Somarelli· 2 shared K. Biswas· 2 shared A. Ghosh· 1 shared A. Mohanty· 1 shared A. N. Saxena· 1 shared

Activity by Year

2019-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 20 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

5 shared papersCancer Biology

M. K. Jolly

Mutual co-authors in cluster

Author profile →

5 papers

Recent·Most cited

The ELF3 transcription factor is associated with an epithelial phenotype and represses epithelial-mesenchymal transition

A. R. Subbalakshmi, S. Sahoo, P. Manjunatha, S. Goyal, V. A. Kasiviswanathan, Y. M, S. R, I. McMullen, J. Somarelli, M. K. Jolly

The paper identifies ELF3 as an epithelial-associated transcription factor that inhibits EMT and stabilizes hybrid E/M phenotypes, with potential prognostic implications in solid tumors.

bioRxiv · Aug 19, 2022Cancer Biology

KLF4 induces Mesenchymal-Epithelial Transition (MET) by suppressing multiple EMT-inducing transcription factors

A. R. Subbalakshmi, S. Sahoo, I. McMullen, A. N. Saxena, S. K. Venugopal, J. Somarelli, M. K. Jolly

This study shows KLF4 suppresses EMT-inducing transcription factors and promotes MET, acting as a potential MET-TF with implications for cancer survival.

Cancers · Oct 13, 2021Peer-reviewedCancer Biology

A computational systems biology approach identifies SLUG as a mediator of partial Epithelial-Mesenchymal Transition (EMT)

A. R. Subbalakshmi, S. Sahoo, K. Biswas, M. K. Jolly

This study identifies SLUG as a stabilizer of hybrid epithelial/mesenchymal phenotypes through computational systems biology analysis.

bioRxiv · Sep 3, 2020Cancer Biology

NFATc acts as a non-canonical phenotypic stability factor for a hybrid epithelial/mesenchymal phenotype

A. R. Subbalakshmi, D. Kundnani, K. Biswas, A. Ghosh, S. Hanash, S. C. Tripathi, M. K. Jolly

This study identifies NFATc as a non-canonical phenotypic stability factor that stabilizes hybrid epithelial/mesenchymal phenotypes by enabling coexistence and transitions between epithelial, mesenchymal, and hybrid states.

bioRxiv · Apr 18, 2020Cancer Biology

A Non-genetic Mechanism for Chemoresistance in Lung Cancer: The Role of Integrin β4/Paxillin Axis

A. Mohanty, A. Nam, A. Pozhitkov, S. Bhattacharya, L. Yang, A. Nathan, X. Wu, S. Srivastava, I. Mambetsariev, M. Nelson, R. Pangeni, D. Raz, Y. Chen, Y. He, J. Orban, , R. Salgia

This study identifies a non-genetic mechanism for cisplatin resistance in lung adenocarcinoma involving the integrin β4/paxillin axis and its regulation of USP1 and VDAC1.

bioRxiv · Sep 25, 2019Cancer Biology