Author

F. Sar

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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Cell Biology· 2 Cancer Biology· 1

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Approach:experimental assay· 2 Organism:human· 2 Research Focus:benchmarking· 1 Assay:bulk RNA-seq· 1 Assay:ChIP-seq· 1 Research Focus:chromatin & epigenetic regulation· 1

Frequent Co-Authors

C. Collins· 3 shared A. Haegert· 1 shared A. Khoeini· 1 shared A. M. Bergman· 1 shared A. Sacayanan· 1 shared B. Gokbayrak· 1 shared B. McConeghy· 1 shared C.-C. F. Huang· 1 shared

Activity by Year

2020-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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3 shared papersCell Biology

C. Collins

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Author profile →

3 papers

Recent·Most cited

scMUSCL: Multi-Source Transfer Learning for Clustering scRNA-seq Data

A. Khoeini, F. Sar, Y.-Y. Lin, C. Collins, M. Ester

scMUSCL improves scRNA-seq clustering by transferring knowledge from multiple annotated datasets without requiring batch correction or prior cluster number knowledge.

bioRxiv · Apr 22, 2024Cell Biology

Patient and cell-type specific hiPSC-modeling of a truncating titin variant associated with atrial fibrillation

K. Huang, M. Ashraf, L. Rohani, Y. Luo, A. Sacayanan, H. Huang, A. Haegert, S. Volik, F. Sar, S. LeBihan, J. Liew, J. D. Roberts, G. F. Tibbits, J. M. Churko, S. Sanatani, , Z. W. Laksman

This study uses patient-derived iPSC-CMs to show that a titin truncating variant increases arrhythmia susceptibility and disrupts sarcomere structure in both atrial and ventricular tissues.

bioRxiv · Mar 2, 2023 · PreprintCell Biology

Functional mapping of androgen receptor enhancer activity

C.-C. F. Huang, S. Lingadahalli, T. Morova, D. Ozturan, E. Hu, I. P. L. Yu, S. Linder, M. Hoogstraat, S. Stelloo, F. Sar, H. van der Poel, U. B. Altintas, M. Saffarzadeh, S. Le Bihan, B. McConeghy, , N. A. Lack

The paper functionally maps AR enhancer activity using STARRseq, finding most AR binding sites are inactive or constitutively active, with inducible enhancers forming regulatory hubs that drive gene transcription.

bioRxiv · Aug 18, 2020Cancer Biology