Author

A. P. Sobinoff

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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Cancer Biology· 2 Cell Biology· 1

Signature Assays, Organisms & Methods

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Organism:human· 3 Research Focus:cancer & tumor microenvironment· 2 Approach:experimental assay· 2 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:drug response / drug discovery· 1 Approach:genetic perturbation / CRISPR· 1 Assay:metabolomics· 1

Frequent Co-Authors

H. A. Pickett· 3 shared A. J. Cesare· 2 shared A. Chambery· 1 shared A. D'Aniello· 1 shared A. H. Porter· 1 shared A. Hsu· 1 shared A. Song· 1 shared B. M. C. Jebaraj· 1 shared

Activity by Year

2022-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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3 shared papersCancer Biology

H. A. Pickett

Mutual co-authors in cluster

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3 papers

Recent·Most cited

Imetelstat-Mediated Alterations in Fatty Acid Metabolism To Induce Ferroptosis As Therapeutic Strategy for Acute Myeloid Leukemia

C. Bruedigam, A. H. Porter, A. Song, G. Vroeg in de Wei, T. Stoll, J. Straube, L. Cooper, G. Cheng, V. F. S. Kahl, A. P. Sobinoff, V. Y. Ling, B. M. C. Jebaraj, Y. Janardhanan, R. Haldar, L. J. Bray, , S. W. Lane

This study identifies ferroptosis as a mechanism by which imetelstat induces therapeutic effects in AML, showing that targeting fatty acid metabolism enhances its efficacy.

bioRxiv · Apr 25, 2023Cancer Biology

Irreversible inhibition of TRF2TRFH recruiting functions: a strategy to induce telomeric replication stress in cancer cells.

A. P. Sobinoff, S. Di Maro, R. R. J. Low, R. Benedetti, S. Tomassi, A. D'Aniello, R. Russo, I. Baglivo, U. Chianese, P. V. Pedone, A. Chambery, A. J. Cesare, L. Altucci, H. A. Pickett, S. Cosconati

This paper identifies APOD53, a covalent cyclic peptide that irreversibly inhibits TRF2TRFH domain function, inducing telomeric replication stress and impairing cancer cell growth.

bioRxiv · Feb 1, 2023 · PreprintCancer Biology

The Eyes Absent family members EYA4 and EYA1 promote PLK1 activation and successful mitosis through tyrosine dephosphorylation.

C. B. Nelson, S. Rogers, K. Roychoudhury, Y. S. Tan, C. J. Atkinson, A. P. Sobinoff, C. G. Tomlinson, A. Hsu, R. Lu, E. Dray, M. Haber, J. I. Fletcher, A. J. Cesare, R. S. Hegde, H. A. Pickett

This study identifies PLK1 as a target of EYA4 and EYA1 phosphatases, showing that dephosphorylation of pY445 promotes PLK1 activation and mitosis, with implications for cancer therapy.

bioRxiv · Oct 10, 2022Cell Biology