E. Blaney Davidson

406 total citations
17 papers, 335 citations indexed

About

E. Blaney Davidson is a scholar working on Molecular Biology, Rheumatology and Pharmacology. According to data from OpenAlex, E. Blaney Davidson has authored 17 papers receiving a total of 335 indexed citations (citations by other indexed papers that have themselves been cited), including 13 papers in Molecular Biology, 11 papers in Rheumatology and 4 papers in Pharmacology. Recurrent topics in E. Blaney Davidson's work include Osteoarthritis Treatment and Mechanisms (11 papers), TGF-β signaling in diseases (8 papers) and Cancer-related molecular mechanisms research (4 papers). E. Blaney Davidson is often cited by papers focused on Osteoarthritis Treatment and Mechanisms (11 papers), TGF-β signaling in diseases (8 papers) and Cancer-related molecular mechanisms research (4 papers). E. Blaney Davidson collaborates with scholars based in Netherlands and India. E. Blaney Davidson's co-authors include WB van den Berg, Alwin Scharstuhl, A. van Caam, P. van der Kraan, P.M. van der Kraan, Wojciech Madej, Marie‐José Goumans, Amaya García de Vinuesa, Peter ten Dijke and Marije I. Koenders and has published in prestigious journals such as Annals of the Rheumatic Diseases, Osteoarthritis and Cartilage and Arthritis Research & Therapy.

In The Last Decade

E. Blaney Davidson

16 papers receiving 328 citations

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
E. Blaney Davidson Netherlands 7 244 169 62 54 39 17 335
Laurence Pesesse Belgium 8 302 1.2× 121 0.7× 78 1.3× 87 1.6× 40 1.0× 12 407
Zelda Plener Belgium 5 282 1.2× 181 1.1× 61 1.0× 48 0.9× 115 2.9× 7 410
Guus van den Akker Netherlands 14 179 0.7× 222 1.3× 91 1.5× 63 1.2× 84 2.2× 36 453
Helen Quasnichka United Kingdom 7 228 0.9× 155 0.9× 71 1.1× 88 1.6× 44 1.1× 11 412
Holly Dupuis Canada 10 155 0.6× 223 1.3× 47 0.8× 47 0.9× 59 1.5× 15 414
A. Khabut Sweden 8 167 0.7× 130 0.8× 55 0.9× 91 1.7× 32 0.8× 12 362
Koichiro Komiya Japan 6 232 1.0× 146 0.9× 68 1.1× 78 1.4× 89 2.3× 10 394
Shanxing Zhang China 12 181 0.7× 174 1.0× 56 0.9× 119 2.2× 59 1.5× 22 465
Zuqiang Wang China 11 141 0.6× 161 1.0× 35 0.6× 28 0.5× 36 0.9× 18 334
Ilona Polur United States 8 286 1.2× 73 0.4× 58 0.9× 40 0.7× 52 1.3× 8 392

Countries citing papers authored by E. Blaney Davidson

Since Specialization
Citations

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

Fields of papers citing papers by E. Blaney Davidson

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by E. Blaney Davidson. 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 E. Blaney Davidson. The network helps show where E. Blaney Davidson may publish in the future.

Co-authorship network of co-authors of E. Blaney Davidson

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

All Works

17 of 17 papers shown
1.
2.
Caam, A. van, et al.. (2019). Transforming growth factor-β dampens interleukin-6 signaling in chondrocytes by decreasing the interleukin-6 receptor. Osteoarthritis and Cartilage. 27. S191–S192. 1 indexed citations
3.
Koenders, Marije I., et al.. (2019). TGF-β dampens IL-6 signaling in articular chondrocytes by decreasing IL-6 receptor expression. Osteoarthritis and Cartilage. 27(8). 1197–1207. 46 indexed citations
4.
Davidson, E. Blaney, et al.. (2019). Pain sensitivity study in the Dutch population: relationship with current pain, gender and sports. Osteoarthritis and Cartilage. 27. S406–S407. 1 indexed citations
5.
Caam, A. van, E. Blaney Davidson, & P. van der Kraan. (2017). TGFβ Signaling Via ALK1 Requires ALK5 Kinase Activity In Chondrocytes. Osteoarthritis and Cartilage. 25. S167–S168. 1 indexed citations
6.
Madej, Wojciech, A. van Caam, E. Blaney Davidson, Pieter Buma, & P.M. van der Kraan. (2016). Unloading results in rapid loss of TGFβ signaling in articular cartilage: role of loading-induced TGFβ signaling in maintenance of articular chondrocyte phenotype?. Osteoarthritis and Cartilage. 24(10). 1807–1815. 31 indexed citations
7.
Akker, Guus van den, et al.. (2016). CRISPR/CAS9 mediated genome engineering of human mesenchymal stem cells. Osteoarthritis and Cartilage. 24. S231–S231. 6 indexed citations
8.
Caam, A. van, Wojciech Madej, Eva Thijssen, et al.. (2016). Expression of TGFβ-family signalling components in ageing cartilage: age-related loss of TGFβ and BMP receptors. Osteoarthritis and Cartilage. 24(7). 1235–1245. 35 indexed citations
9.
10.
Caam, A. van, E. Blaney Davidson, Amaya García de Vinuesa, et al.. (2015). The high affinity ALK1-ligand BMP9 induces a hypertrophy-like state in chondrocytes that is antagonized by TGFβ1. Osteoarthritis and Cartilage. 23(6). 985–995. 29 indexed citations
11.
Davidson, E. Blaney, et al.. (2015). A4.6 TGF-β is a potent inducer of nerve growth factor in articular cartilage via the ALK5-SMAD2/3 pathway. Potential role in OA related pain?. Annals of the Rheumatic Diseases. 74. A38–A38. 1 indexed citations
12.
Caam, A. van, E. Blaney Davidson, Eva Thijssen, WB van den Berg, & P. van der Kraan. (2014). Age-related loss of the transforming growth factor β receptor ALK5 precedes osteoarthritis development in cartilage. Osteoarthritis and Cartilage. 22. S57–S57. 1 indexed citations
13.
Davidson, E. Blaney, et al.. (2013). Synovial Wnt and WISP1 expression induces cartilage damage by skewing of TGF-beta signaling via the canonical Wnt signaling pathway. Osteoarthritis and Cartilage. 21. S54–S54. 1 indexed citations
14.
Caam, A. van, E. Blaney Davidson, Wojciech Madej, WB van den Berg, & P. van der Kraan. (2013). Pronounced decrease in expression of chondroprotective Smad2/3 phosphorylating TGFβ-signaling receptors during ageing in healthy cartilage. Osteoarthritis and Cartilage. 21. S130–S130. 1 indexed citations
15.
Caam, A. van, E. Blaney Davidson, E.L. Vitters, WB van den Berg, & P. van der Kraan. (2012). BMP-9 induces both smad1/5/8 and Smad2/3 phosphorylation, and specific response genes, in chondrocytes. Osteoarthritis and Cartilage. 20. S133–S133. 1 indexed citations
16.
Caam, A. van, E. Blaney Davidson, E.L. Vitters, WB van den Berg, & P. van der Kraan. (2012). AB0119 BMP-9 induces both SMAD1/5/8 and SMAD2/3 phosphorylation, and specific response genes, in chondrocytes. Annals of the Rheumatic Diseases. 71. 644–644. 1 indexed citations
17.
Davidson, E. Blaney, et al.. (2005). Reduced transforming growth factor-beta signaling in cartilage of old mice: role in impaired repair capacity. Arthritis Research & Therapy. 7(6). R1338–47. 164 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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