James R. Cavey

1.2k total citations
16 papers, 910 citations indexed

About

James R. Cavey is a scholar working on Molecular Biology, Oncology and Cancer Research. According to data from OpenAlex, James R. Cavey has authored 16 papers receiving a total of 910 indexed citations (citations by other indexed papers that have themselves been cited), including 14 papers in Molecular Biology, 12 papers in Oncology and 4 papers in Cancer Research. Recurrent topics in James R. Cavey's work include Ubiquitin and proteasome pathways (11 papers), Cancer-related Molecular Pathways (8 papers) and Bone health and treatments (4 papers). James R. Cavey is often cited by papers focused on Ubiquitin and proteasome pathways (11 papers), Cancer-related Molecular Pathways (8 papers) and Bone health and treatments (4 papers). James R. Cavey collaborates with scholars based in United Kingdom, United States and Sweden. James R. Cavey's co-authors include Robert Layfield, Mark S. Searle, Paul W. Sheppard, Stuart H. Ralston, Barbara Ciani, Jed Long, James Lowe, Lynne J. Hocking, Barry Shaw and Alice Goode and has published in prestigious journals such as Journal of Biological Chemistry, Biochemistry and FEBS Letters.

In The Last Decade

James R. Cavey

16 papers receiving 900 citations

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
James R. Cavey United Kingdom 13 558 360 299 133 129 16 910
Hirotaka Matsumura Japan 8 577 1.0× 146 0.4× 143 0.5× 98 0.7× 22 0.2× 9 880
Rodney J. Moreland United States 12 903 1.6× 215 0.6× 184 0.6× 135 1.0× 42 0.3× 19 1.3k
Patricia Vusio France 12 434 0.8× 337 0.9× 46 0.2× 69 0.5× 10 0.1× 16 903
Beatrice Cardinali Italy 20 1.0k 1.8× 100 0.3× 34 0.1× 53 0.4× 58 0.4× 37 1.2k
S. Hardy United States 3 473 0.8× 137 0.4× 60 0.2× 70 0.5× 7 0.1× 6 729
Maureen Mee United Kingdom 11 412 0.7× 108 0.3× 135 0.5× 167 1.3× 115 0.9× 14 678
Irina Lassot France 15 1.3k 2.3× 296 0.8× 156 0.5× 282 2.1× 38 0.3× 19 1.5k
Haiqing Yi United States 19 533 1.0× 81 0.2× 73 0.2× 154 1.2× 50 0.4× 34 851
Toshikazu Nagao Japan 9 562 1.0× 283 0.8× 115 0.4× 113 0.8× 13 0.1× 12 731
Katsuhiro Sasaki Japan 14 987 1.8× 352 1.0× 222 0.7× 258 1.9× 66 0.5× 23 1.5k

Countries citing papers authored by James R. Cavey

Since Specialization
Citations

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

Fields of papers citing papers by James R. Cavey

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of James R. Cavey

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

All Works

16 of 16 papers shown
1.
Begitt, Andreas, et al.. (2023). A family-wide assessment of latent STAT transcription factor interactions reveals divergent dimer repertoires. Journal of Biological Chemistry. 299(5). 104703–104703. 4 indexed citations
2.
Goode, Alice, Jed Long, James R. Cavey, et al.. (2016). Defective recognition of LC3B by mutant SQSTM1/p62 implicates impairment of autophagy as a pathogenic mechanism in ALS-FTLD. Autophagy. 12(7). 1094–1104. 116 indexed citations
3.
Bolt, Edward L., et al.. (2015). Identification of Escherichia coli ygaQ and rpmG as novel mitomycin C resistance factors implicated in DNA repair. Bioscience Reports. 36(1). e00290–e00290. 4 indexed citations
4.
Searle, Mark S., Thomas P. Garner, Joanna Strachan, et al.. (2012). Structural insights into specificity and diversity in mechanisms of ubiquitin recognition by ubiquitin-binding domains. Biochemical Society Transactions. 40(2). 404–408. 15 indexed citations
5.
Garner, Thomas P., Joanna Strachan, Jed Long, et al.. (2011). Independent Interactions of Ubiquitin-Binding Domains in a Ubiquitin-Mediated Ternary Complex. Biochemistry. 50(42). 9076–9087. 28 indexed citations
6.
Heinen, Christian, Thomas P. Garner, Jed Long, et al.. (2010). Mutant p62/SQSTM1 UBA domains linked to Paget's disease of bone differ in their abilities to function as stabilization signals. FEBS Letters. 584(8). 1585–1590. 12 indexed citations
7.
Paine, Simon, Lynn Bedford, Julian R. Thorpe, et al.. (2009). Immunoreactivity to Lys63-linked polyubiquitin is a feature of neurodegeneration. Neuroscience Letters. 460(3). 205–208. 34 indexed citations
8.
Garner, Thomas P., Thilo Hagen, Barry Shaw, et al.. (2008). Characterization of a Non-UBA Domain Missense Mutation of Sequestosome 1 (SQSTM1) in Paget's Disease of Bone. Journal of Bone and Mineral Research. 24(4). 632–642. 44 indexed citations
9.
Long, Jed, James R. Cavey, Paul W. Sheppard, et al.. (2007). Ubiquitin Recognition by the Ubiquitin-associated Domain of p62 Involves a Novel Conformational Switch. Journal of Biological Chemistry. 283(9). 5427–5440. 128 indexed citations
10.
Cavey, James R., Stuart H. Ralston, Paul W. Sheppard, et al.. (2006). Loss of Ubiquitin Binding Is a Unifying Mechanism by Which Mutations of SQSTM1 Cause Paget’s Disease of Bone. Calcified Tissue International. 78(5). 271–277. 63 indexed citations
11.
Layfield, Robert, James R. Cavey, Joanna Long, et al.. (2006). p62 mutations, ubiquitin recognition and Paget's disease of bone. Biochemical Society Transactions. 34(5). 735–737. 22 indexed citations
12.
Cavey, James R., Stuart H. Ralston, Lynne J. Hocking, et al.. (2005). Loss of Ubiquitin-Binding Associated With Paget's Disease of Bone p62 (SQSTM1) Mutations. Journal of Bone and Mineral Research. 20(4). 619–624. 94 indexed citations
13.
Layfield, Robert, Barbara Ciani, Stuart H. Ralston, et al.. (2004). Structural and functional studies of mutations affecting the UBA domain of SQSTM1 (p62) which cause Paget's disease of bone. Biochemical Society Transactions. 32(5). 728–730. 27 indexed citations
14.
Hocking, Lynne J., Gavin Lucas, Anna Daroszewska, et al.. (2004). Novel UBA Domain Mutations of SQSTM1 in Paget's Disease of Bone: Genotype Phenotype Correlation, Functional Analysis, and Structural Consequences. Journal of Bone and Mineral Research. 19(7). 1122–1127. 124 indexed citations
15.
Layfield, Robert, James R. Cavey, & James Lowe. (2003). Role of ubiquitin-mediated proteolysis in the pathogenesis of neurodegenerative disorders. Ageing Research Reviews. 2(4). 343–356. 87 indexed citations
16.
Ciani, Barbara, Robert Layfield, James R. Cavey, Paul W. Sheppard, & Mark S. Searle. (2003). Structure of the Ubiquitin-associated Domain of p62 (SQSTM1) and Implications for Mutations That Cause Paget's Disease of Bone. Journal of Biological Chemistry. 278(39). 37409–37412. 108 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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