Author

Tzah Feldman

Weizmann Institute of ScienceORCID 0000-0002-6699-8315Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Assay:DNA methylation· 2 Organism:human· 2 Assay:CRISPR screen· 1 Research Focus:differential expression· 1 Approach:experimental assay· 1 Approach:statistical model· 1 Research Focus:variant calling· 1

Frequent Co-Authors

Liran I. ShlushiD· 2 shared Nathali KaushanskyiD· 2 shared Noa Chapal-Ilani· 2 shared Yoni MoskovitziD· 2 shared Aditee KadamiD· 1 shared Akhiad Bercovich· 1 shared Amanda MitchelliD· 1 shared Amos TanayiD· 1 shared

Activity by Year

2020-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 36 mutual co-author links

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2 shared papersGenetics

Liran I. ShlushORCID

Mutual co-authors in cluster

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2 papers

Recent·Most cited

DNA Methylation is stable after MMEJ and NHEJ double strand break repair

Ester Bnaya, Shay Shilo, Tzah Feldman, Tal Bacharach, Yoni Moskovitz, Aditee Kadam, Paz Yedidim, Hadas Azogy, Nathali Kaushansky, Noa Chapal-Ilani, Liran I. Shlush

The paper examines DNA methylation stability after MMEJ and NHEJ repair mechanisms, finding that methylation levels remain stable despite repair-induced deletions and in the presence of a DNMT3A mutation.

bioRxiv · Jul 21, 2022 · PreprintGenetics

Recurrent pre-leukemic deletions in myeloid malignancies are the result of DNA double-strand breaks followed by microhomology-mediated end joining

Tzah Feldman, Akhiad Bercovich, Yoni Moskovitz, Noa Chapal-Ilani, Amanda Mitchell, Jessie J.F. Medeiros, Nathali Kaushansky, Tamir Biezuner, Mark David Minden, Vikas K Gupta, Amos Tanay, Liran I. Shlush

The paper identifies microhomology-mediated end joining (MMEJ) as the mechanism behind recurrent deletions in myeloid malignancies and shows that these deletions occur in multipotent hematopoietic stem cells.

bioRxiv · Jan 1, 2020 · PreprintGenomics