Daniel Esch

584 total citations
9 papers, 429 citations indexed

About

Daniel Esch is a scholar working on Molecular Biology, Public Health, Environmental and Occupational Health and Genetics. According to data from OpenAlex, Daniel Esch has authored 9 papers receiving a total of 429 indexed citations (citations by other indexed papers that have themselves been cited), including 9 papers in Molecular Biology, 2 papers in Public Health, Environmental and Occupational Health and 1 paper in Genetics. Recurrent topics in Daniel Esch's work include Pluripotent Stem Cells Research (8 papers), CRISPR and Genetic Engineering (6 papers) and Genomics and Chromatin Dynamics (4 papers). Daniel Esch is often cited by papers focused on Pluripotent Stem Cells Research (8 papers), CRISPR and Genetic Engineering (6 papers) and Genomics and Chromatin Dynamics (4 papers). Daniel Esch collaborates with scholars based in Germany, Singapore and Spain. Daniel Esch's co-authors include Hans R. Schöler, Marcos J. Araúzo‐Bravo, Vlad Cojocaru, Ralf Jauch, Guangming Wu, Dong‐Wook Han, Natàlia Tàpia, Juha Vahokoski, Matthew R. Groves and Vivian Pogenberg and has published in prestigious journals such as Nature, Nature Communications and PLoS ONE.

In The Last Decade

Daniel Esch

9 papers receiving 421 citations

Peers — A (Enhanced Table)

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

Name	h						Papers	Cites
Daniel Esch Germany	8	402	54	27	25	20	9	429
Yasunao Kamikawa Japan	10	452 1.1×	50 0.9×	32 1.2×	29 1.2×	10 0.5×	18	513
Sicong Zeng China	10	297 0.7×	42 0.8×	77 2.9×	21 0.8×	25 1.3×	28	356
Diana Guallar Spain	12	402 1.0×	44 0.8×	31 1.1×	49 2.0×	21 1.1×	23	444
Christine Gran Neurauter Norway	9	280 0.7×	51 0.9×	29 1.1×	40 1.6×	8 0.4×	11	320
Andrew Perez United States	7	349 0.9×	90 1.7×	21 0.8×	48 1.9×	9 0.5×	8	394
Valentina Guasconi France	10	354 0.9×	58 1.1×	35 1.3×	34 1.4×	11 0.6×	11	378
Amandine Bemmo Canada	6	244 0.6×	51 0.9×	22 0.8×	53 2.1×	11 0.6×	8	294
Bobbie Pelham‐Webb United States	6	448 1.1×	52 1.0×	11 0.4×	30 1.2×	9 0.5×	7	468
Teresa Olbrich United States	8	243 0.6×	51 0.9×	24 0.9×	14 0.6×	12 0.6×	10	305
Thomas L. Clarke United States	12	391 1.0×	37 0.7×	64 2.4×	48 1.9×	12 0.6×	14	472

Countries citing papers authored by Daniel Esch

Since Specialization

Citations

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

Fields of papers citing papers by Daniel Esch

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Daniel Esch. 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 Daniel Esch. The network helps show where Daniel Esch may publish in the future.

Co-authorship network of co-authors of Daniel Esch

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

All Works

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9 of 9 papers shown

1.

Wu, Guangming, Marcos J. Araúzo‐Bravo, Daniel Esch, et al.. (2016). Changing POU dimerization preferences converts Oct6 into a pluripotency inducer. EMBO Reports. 18(2). 319–333. 37 indexed citations

2.

Tàpia, Natàlia, Caitlin M. MacCarthy, Daniel Esch, et al.. (2015). Dissecting the role of distinct OCT4-SOX2 heterodimer configurations in pluripotency. Scientific Reports. 5(1). 13533–13533. 51 indexed citations

3.

Singhal, Nishant, Daniel Esch, Martin Stehling, & Hans R. Schöler. (2014). BRG1 Is Required to Maintain Pluripotency of Murine Embryonic Stem Cells. BioResearch open access. 3(1). 1–8. 17 indexed citations

4.

Pijnappel, W.W.M. Pim, Daniel Esch, Marijke Baltissen, et al.. (2013). A central role for TFIID in the pluripotent transcription circuitry. Nature. 495(7442). 516–519. 64 indexed citations

5.

Esch, Daniel, Juha Vahokoski, Matthew R. Groves, et al.. (2013). A unique Oct4 interface is crucial for reprogramming to pluripotency. Nature Cell Biology. 15(3). 295–301. 126 indexed citations

6.

Klein, Diana, Guangming Wu, Daniel Esch, et al.. (2012). Zfp296 Is a Novel, Pluripotent-Specific Reprogramming Factor. PLoS ONE. 7(4). e34645–e34645. 31 indexed citations

7.

Tàpia, Natàlia, Peter Reinhardt, Guangming Wu, et al.. (2012). Reprogramming to pluripotency is an ancient trait of vertebrate Oct4 and Pou2 proteins. Nature Communications. 3(1). 1279–1279. 57 indexed citations

8.

Esch, Daniel, et al.. (2011). Visualization and Exploration of Conserved Regulatory Modules Using ReXSpecies 2. BMC Evolutionary Biology. 11(1). 267–267. 3 indexed citations

9.

Sebastiano, Vittorio, Mathieu Dalvai, Luca Gentile, et al.. (2010). Oct1 regulates trophoblast development during early mouse embryogenesis. Development. 137(21). 3551–3560. 43 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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