Author

Balajikarthick Subramanian

Beth Israel Deaconess Medical CenterORCID 0000-0001-6807-0257Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Genetics· 1 Pathology· 1

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Approach:experimental assay· 2 Assay:proteomics· 2 Research Focus:cell signaling & trafficking· 1 Organism:human· 1 Organism:mouse· 1 Approach:statistical model· 1

Frequent Co-Authors

Martin R. PollakiD· 2 shared Seth L. AlperiD· 2 shared Chandra Perez· 1 shared Cristian V. RiellaiD· 1 shared Henry Higgs· 1 shared Henry N. HiggsiD· 1 shared Isaac Stillman· 1 shared Johannes Schlondorff· 1 shared

Activity by Year

2019-2024 · peak 1/yr

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10 top collaborators · 30 mutual co-author links

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2 shared papersGenetics

Martin R. PollakORCID

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2 papers

Recent·Most cited

GeneticsbioRxivPreprintJun 8, 2024

Missense Mutant Gain-of-Function Causes Inverted Formin 2 (INF2)-Related Focal Segmental Glomerulosclerosis (FSGS)

Balajikarthick Subramanian, Sarah Williams, Sophie Karp…·Martin R. Pollak

This study shows that a gain-of-function INF2 mutation causes FSGS in mice, linking INF2's cellular roles to disease progression and explaining its autosomal dominant inheritance.

4 citations

mouseproteomics

𝕏 PostBluesky

PathologybioRxivPreprintJan 26, 2019

Proteolytic program-dependent functions are impaired in INF2-mediated focal segmental glomerulosclerosis.

Balajikarthick Subramanian, Justin Chun, Chandra Perez…·Martin R. Pollak

This study identifies a proteolytic cleavage mechanism in INF2 that affects its function in podocytes, leading to impaired localization and contributing to FSGS.

DOI 10.1101/530642

humanproteomics

𝕏 PostBluesky