James M. Dewar

1.8k total citations
31 papers, 1.3k citations indexed

About

James M. Dewar is a scholar working on Molecular Biology, Cell Biology and Endocrinology, Diabetes and Metabolism. According to data from OpenAlex, James M. Dewar has authored 31 papers receiving a total of 1.3k indexed citations (citations by other indexed papers that have themselves been cited), including 21 papers in Molecular Biology, 6 papers in Cell Biology and 5 papers in Endocrinology, Diabetes and Metabolism. Recurrent topics in James M. Dewar's work include DNA Repair Mechanisms (17 papers), CRISPR and Genetic Engineering (8 papers) and Microtubule and mitosis dynamics (6 papers). James M. Dewar is often cited by papers focused on DNA Repair Mechanisms (17 papers), CRISPR and Genetic Engineering (8 papers) and Microtubule and mitosis dynamics (6 papers). James M. Dewar collaborates with scholars based in United States, United Kingdom and Netherlands. James M. Dewar's co-authors include Johannes C. Walter, David Lydall, Magda Budzowska, Julien P. Duxin, Hasan Yardimci, Martin A. Cohn, Jieqiong Zhang, Matthias Mann, Markus Räschle and Wouter Koole and has published in prestigious journals such as Nature, Cell and Nucleic Acids Research.

In The Last Decade

James M. Dewar

29 papers receiving 1.3k citations

Peers — A (Enhanced Table)

Peers by citation overlap · career bar shows stage (early→late) cites · hero ref

Name	h						Papers	Cites
James M. Dewar United States	18	1.1k	252	153	135	120	31	1.3k
Melissa S. McNulty United States	13	470 0.4×	98 0.4×	89 0.6×	59 0.4×	88 0.7×	19	702
Huifang Dai China	16	1.1k 1.0×	71 0.3×	210 1.4×	64 0.5×	80 0.7×	27	1.3k
Daisheng Song United States	16	509 0.5×	91 0.4×	27 0.2×	50 0.4×	177 1.5×	21	970
Huiling Zheng China	11	532 0.5×	42 0.2×	105 0.7×	18 0.1×	40 0.3×	48	745
Joon Hyeok Kwak United States	10	307 0.3×	54 0.2×	57 0.4×	23 0.2×	29 0.2×	20	568
Takayuki Kurihara Japan	17	607 0.6×	73 0.3×	123 0.8×	280 2.1×	60 0.5×	34	1.1k
Anabel Rojas Spain	22	830 0.8×	72 0.3×	72 0.5×	127 0.9×	264 2.2×	39	1.3k
Ekaterini A. Kritikou Canada	13	435 0.4×	36 0.1×	228 1.5×	15 0.1×	71 0.6×	18	780
Chenming Xu China	17	446 0.4×	34 0.1×	40 0.3×	69 0.5×	295 2.5×	92	1.1k
Marta Martı́n Spain	16	549 0.5×	70 0.3×	112 0.7×	95 0.7×	92 0.8×	30	849

Countries citing papers authored by James M. Dewar

Since Specialization

Citations

This map shows the geographic impact of James M. Dewar'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 James M. Dewar with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites James M. Dewar more than expected).

Fields of papers citing papers by James M. Dewar

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by James M. Dewar. 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 James M. Dewar. The network helps show where James M. Dewar may publish in the future.

Co-authorship network of co-authors of James M. Dewar

This figure shows the co-authorship network connecting the top 25 collaborators of James M. Dewar. A scholar is included among the top collaborators of James M. Dewar 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 James M. Dewar. James M. Dewar is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

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20 of 20 papers shown

Cortez, David, et al.. (2025). Leading and lagging strand abasic sites differentially affect vertebrate replisome progression but involve analogous bypass mechanisms. Nucleic Acids Research. 53(18).

Dewar, James M., et al.. (2024). Control of DNA replication in vitro using a reversible replication barrier. Nature Protocols. 19(7). 1940–1983. 2 indexed citations

Heintzman, Darren R., et al.. (2023). RTEL1 and MCM10 overcome topological stress during vertebrate replication termination. Cell Reports. 42(2). 112109–112109. 12 indexed citations

Liu, Wenpeng, et al.. (2023). Replication fork uncoupling causes nascent strand degradation and fork reversal. Nature Structural & Molecular Biology. 30(1). 115–124. 19 indexed citations

Mehta, Kavi P.M., Jo Ann W. Byl, Runxiang Zhao, et al.. (2022). Topoisomerase II poisons inhibit vertebrate DNA replication through distinct mechanisms. The EMBO Journal. 41(12). e110632–e110632. 21 indexed citations

Dewar, James M., et al.. (2022). Approaches to Monitor Termination of DNA Replication Using Xenopus Egg Extracts. Methods in molecular biology. 2444. 105–123.

Dewar, James M., et al.. (2021). Single-strand DNA breaks cause replisome disassembly. Molecular Cell. 81(6). 1309–1318.e6. 76 indexed citations

Parisis, Nikolaos, Liliana Krasińska, Serge Urbach, et al.. (2017). Initiation of DNA replication requires actin dynamics and formin activity. The EMBO Journal. 36(21). 3212–3231. 72 indexed citations

Dewar, James M., et al.. (2017). CRL2^Lrr1 promotes unloading of the vertebrate replisome from chromatin during replication termination. Genes & Development. 31(3). 275–290. 87 indexed citations

10.

Dewar, James M. & Johannes C. Walter. (2017). Mechanisms of DNA replication termination. Nature Reviews Molecular Cell Biology. 18(8). 507–516. 100 indexed citations

11.

Dewar, James M., Magda Budzowska, & Johannes C. Walter. (2015). The mechanism of DNA replication termination in vertebrates. Nature. 525(7569). 345–350. 116 indexed citations

12.

Duxin, Julien P., James M. Dewar, Hasan Yardimci, & Johannes C. Walter. (2014). Repair of a DNA-Protein Crosslink by Replication-Coupled Proteolysis. Cell. 159(2). 346–357. 189 indexed citations

13.

Segura‐Bayona, Sandra, et al.. (2014). FANCJ promotes DNA synthesis through G‐quadruplex structures. The EMBO Journal. 33(21). 2521–2533. 115 indexed citations

14.

Dewar, James M. & David Lydall. (2012). Simple, Non-radioactive Measurement of Single-Stranded DNA at Telomeric, Sub-telomeric, and Genomic Loci in Budding Yeast. Methods in molecular biology. 920. 341–348. 9 indexed citations

15.

Dewar, James M. & David Lydall. (2010). Pif1- and Exo1-dependent nucleases coordinate checkpoint activation following telomere uncapping. The EMBO Journal. 29(23). 4020–4034. 64 indexed citations

16.

Daniels, Mark, et al.. (1991). Actions of L-363,586, a cyclic hexapeptide analogue of somatostatin, on GH secretion by human somatotrophinoma cells in vitro. Life Sciences. 49(16). 1207–1212. 2 indexed citations

17.

Daniels, Mark, et al.. (1991). Effects of insulin-like growth factor-II on growth hormone release from human somatotrophinoma cells in vitro. Journal of Endocrinology. 129(3). 447–451. 4 indexed citations

18.

White, M. C., Mark Daniels, Philip L. Newland, et al.. (1990). LH AND FSH SECRETION AND RESPONSES TO GnRH AND TRH IN PATIENTS WITH CLINICALLY FUNCTIONLESS PITUITARY ADENOMAS. Clinical Endocrinology. 32(6). 681–688. 18 indexed citations

19.

Mk, Ward, et al.. (1977). Ionised calcium during haemodialysis.. Munich Personal RePEc Archive (Ludwig Maximilian University of Munich). 14. 229–35. 1 indexed citations

20.

Hersch, C., et al.. (1971). A double-blind trial in hypertension comparing Baycaron (FBA 1500), hydrochlorothiazide and placebo.. PubMed. 45(12). 323–323. 8 indexed citations

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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