Velibor Savic

1.6k total citations · 1 hit paper
15 papers, 1.2k citations indexed

About

Velibor Savic is a scholar working on Molecular Biology, Oncology and Cell Biology. According to data from OpenAlex, Velibor Savic has authored 15 papers receiving a total of 1.2k indexed citations (citations by other indexed papers that have themselves been cited), including 15 papers in Molecular Biology, 5 papers in Oncology and 4 papers in Cell Biology. Recurrent topics in Velibor Savic's work include DNA Repair Mechanisms (11 papers), Genomics and Chromatin Dynamics (5 papers) and DNA and Nucleic Acid Chemistry (3 papers). Velibor Savic is often cited by papers focused on DNA Repair Mechanisms (11 papers), Genomics and Chromatin Dynamics (5 papers) and DNA and Nucleic Acid Chemistry (3 papers). Velibor Savic collaborates with scholars based in United Kingdom, United States and Denmark. Velibor Savic's co-authors include Simon Bekker‐Jensen, Claudia Lukas, Jiří Bártek, Beate Neumann, Kok‐Lung Chan, Ian D. Hickson, Craig H. Bassing, Bu Yin, Katherine Yang‐Iott and Andrea Bredemeyer and has published in prestigious journals such as Cell, The Journal of Experimental Medicine and Blood.

In The Last Decade

Velibor Savic

14 papers receiving 1.2k citations

Hit Papers

align trajectories

What are hit papers?

Hit papers significantly outperform the citation benchmark for their cohort. A paper qualifies if it has ≥500 total citations, achieves ≥1.5× the top-1% citation threshold for papers in the same subfield and year (this is the minimum needed to enter the top 1%, not the average within it), or reaches the top citation threshold in at least one of its specific research topics.

53BP1 nuclear bodies form around DNA lesions generated by mitotic transmission of chromosomes under replication stress

2011 520 citations Claudia Lukas, Velibor Savic et al. Nature Cell Biology profile →

Peers

Countries citing papers authored by Velibor Savic

Since Specialization

Citations

This map shows the geographic impact of Velibor Savic's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Velibor Savic with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Velibor Savic more than expected).

Fields of papers citing papers by Velibor Savic

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Velibor Savic. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Velibor Savic. The network helps show where Velibor Savic may publish in the future.

Co-authorship network of co-authors of Velibor Savic

This figure shows the co-authorship network connecting the top 25 collaborators of Velibor Savic. A scholar is included among the top collaborators of Velibor Savic based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Velibor Savic. Velibor Savic is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

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15 of 15 papers shown

#	Work	Indexed citations
1	Large XPF-dependent deletions following misrepair of a DNA double strand break are prevented by the RNA:DNA helicase Senataxin 2018 ·Scientific Reports ·(unknown), (unknown), Natalia Gromak, Velibor Savic, Steve M. M. Sweet	24
2	HECTD3 Mediates an HSP90-Dependent Degradation Pathway for Protein Kinase Clients 2017 ·Cell Reports ·Zhaobo Li, Lihong Zhou, Chrisostomos Prodromou, Velibor Savic, Laurence H. Pearl	23
3	Novel synthetic lethality screening method identifies TIP60-dependent radiation sensitivity in the absence of BAF180 2016 ·DNA repair ·(unknown), Grant A. McGregor, Johanne M. Murray, Jessica A. Downs, Velibor Savic	8
4	A first generation inhibitor of human Greatwall kinase, enabled by structural and functional characterisation of a minimal kinase domain construct 2016 ·Oncotarget ·Cory A. Ocasio, (unknown), Sarah Walker, (unknown), John Spencer, Frances M. G. Pearl, Simon E. Ward, Velibor Savic, Laurence H. Pearl, Helfrid Hochegger, Antony W. Oliver	30
5	TRIP12 and UBR5 Suppress Spreading of Chromatin Ubiquitylation at Damaged Chromosomes 2014 ·Cell ·Þorkell Guðjόnsson, Matthias Altmeyer, Velibor Savic, (unknown), Christoffel Dinant, (unknown), Jiřina Bártková, Maria Poulsen, Yasuyoshi Oka, Simon Bekker‐Jensen, Niels Mailand, Beate Neumann, Jean-Karim Hèriché, Robert Shearer, Darren N. Saunders, Jiří Bártek, (unknown), Claudia Lukas	2
6	Do chromatin changes around a nascent double strand DNA break spread spherically into linearly non-adjacent chromatin? 2013 ·Frontiers in Genetics ·Velibor Savic	2
7	TRIP12 and UBR5 Suppress Spreading of Chromatin Ubiquitylation at Damaged Chromosomes 2012 ·Cell ·Þorkell Guðjόnsson, Matthias Altmeyer, Velibor Savic, Luis Toledo, Christoffel Dinant, (unknown), Jiřina Bártková, Maria Poulsen, Yasuyoshi Oka, Simon Bekker‐Jensen, Niels Mailand, Beate Neumann, Jean-Karim Hèriché, Robert F. Shearer, Darren N. Saunders, Jiří Bártek, (unknown), Claudia Lukas	262
8	53BP1 nuclear bodies form around DNA lesions generated by mitotic transmission of chromosomes under replication stress breakdown → 2011 ·Nature Cell Biology ·Claudia Lukas, Velibor Savic, Simon Bekker‐Jensen, (unknown), Beate Neumann, (unknown), (unknown), Kok‐Lung Chan, Ian D. Hickson, Jiří Bártek, (unknown)	520
9	Chromatin Binding of SRp20 and ASF/SF2 and Dissociation from Mitotic Chromosomes Is Modulated by Histone H3 Serine 10 Phosphorylation 2009 ·Molecular Cell ·Rebecca J. Loomis, Yoshinori Naoe, J. Brandon Parker, Velibor Savic, (unknown), Todd S. Macfarlan, James L. Manley, Debabrata Chakravarti	147
10	Formation of Dynamic γ-H2AX Domains along Broken DNA Strands Is Distinctly Regulated by ATM and MDC1 and Dependent upon H2AX Densities in Chromatin 2009 ·Molecular Cell ·Velibor Savic, Bu Yin, Nancy L. Maas, Andrea Bredemeyer, Andrea C. Carpenter, Beth A. Helmink, Katherine Yang‐Iott, Barry P. Sleckman, Craig H. Bassing	161
11	Chipping away at γ-H2AX foci 2009 ·Cell Cycle ·Velibor Savic, Keri B. Sanborn, Jordan S. Orange, Craig H. Bassing	7
12	Histone H2AX stabilizes broken DNA strands to suppress chromosome breaks and translocations during V(D)J recombination 2009 ·The Journal of Experimental Medicine ·Bu Yin, Velibor Savic, Marisa M. Juntilla, Andrea Bredemeyer, Katherine Yang‐Iott, Beth A. Helmink, Gary A. Koretzky, Barry P. Sleckman, Craig H. Bassing	42
13	H2ax/p53-deficient thymic lymphomas with clonal translocations Aberrant V(D)J recombination is not required for rapid development of 2008 ·Craig H. Bassing, Sheila Ranganath, (unknown), Velibor Savic, (unknown), William C. Frederick	0
14	ATM prevents unattended DNA double strand breaks on site and in generations to come 2007 ·Cancer Biology & Therapy ·Bu Yin, Velibor Savic, Craig H. Bassing	6
15	Aberrant V(D)J recombination is not required for rapid development of H2ax/p53-deficient thymic lymphomas with clonal translocations 2007 ·Blood ·Craig H. Bassing, Sheila Ranganath, (unknown), Velibor Savic, (unknown), Frederick W. Alt	14

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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