Author

T. Stankovic

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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Biochemistry· 1 Cancer Biology· 1 Cell Biology· 1

Signature Assays, Organisms & Methods

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Research Focus:drug response / drug discovery· 2 Approach:experimental assay· 2 Organism:bacteria (other)· 1 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:chromatin & epigenetic regulation· 1 Approach:genetic perturbation / CRISPR· 1

Frequent Co-Authors

A. Barros· 1 shared A. Bradley· 1 shared A. Kossenkov· 1 shared A. Peracchi· 1 shared A. SRIVASTAVA· 1 shared A. Stanojevic· 1 shared A. Welm· 1 shared B. A. Van Tine· 1 shared

Activity by Year

2018-2020 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 22 mutual co-author links

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1 shared paperCell Biology

A. Barros

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

(R)-1-hydroxy-2-aminoethylphosphonate ammonia-lyase, a new PLP-dependent enzyme involved in bacterial phosphonate degradation

E. Zangelmi, T. Stankovic, M. Malatesta, D. Acquotti, K. Pallitsch, A. Peracchi

This study identifies PbfA as a novel PLP-dependent enzyme that catalyzes the elimination of (R)-1-hydroxy-2-aminoethylphosphonate to generate phosphonoacetaldehyde, expanding the bacterial phosphonate degradation pathway.

bioRxiv · Dec 13, 2020Biochemistry

Systematic Establishment of Robustness and Standards in Patient-Derived Xenograft Experiments and Analysis

Y. A. Evrard, A. SRIVASTAVA, J. Randjelovic, S. Arunachalam, C. J. Bult, H. Chen, L. Chen, M. Davies, S. Davies, B. Davis-Dusenbery, J. DiGiovanna, L. Ding, J. H. Doroshow, B. Fang, C. Frech, , J. Morris

The paper tests the reproducibility of PDX drug responses and sequence results across different labs using standardized protocols and workflows.

bioRxiv · Oct 2, 2019Cancer Biology

ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks

G. Balmus, D. Pilger, J. Coates, M. Demir, M. Sczaniecka-Clift, A. Barros, M. Woods, B. Fu, F. Yang, E. Chen, M. Ostermaier, T. Stankovic, H. Ponstingl, M. Herzog, K. Yusa, , S. P. P. Jackson

The paper identifies how ATM counteracts toxic non-homologous end-joining at broken replication forks by showing that loss of NHEJ components or BRCA1-A complex confers resistance to DNA-damaging agents in ATM-deficient cells.

bioRxiv · May 24, 2018Cell Biology