John G. Shelton

1.1k total citations
17 papers, 929 citations indexed

About

John G. Shelton is a scholar working on Molecular Biology, Oncology and Pulmonary and Respiratory Medicine. According to data from OpenAlex, John G. Shelton has authored 17 papers receiving a total of 929 indexed citations (citations by other indexed papers that have themselves been cited), including 12 papers in Molecular Biology, 9 papers in Oncology and 3 papers in Pulmonary and Respiratory Medicine. Recurrent topics in John G. Shelton's work include PI3K/AKT/mTOR signaling in cancer (6 papers), Cytokine Signaling Pathways and Interactions (6 papers) and Melanoma and MAPK Pathways (5 papers). John G. Shelton is often cited by papers focused on PI3K/AKT/mTOR signaling in cancer (6 papers), Cytokine Signaling Pathways and Interactions (6 papers) and Melanoma and MAPK Pathways (5 papers). John G. Shelton collaborates with scholars based in United States, Italy and Germany. John G. Shelton's co-authors include James A. McCubrey, Linda S. Steelman, Richard A. Franklin, William L. Blalock, John Tayu Lee, Fumin Chang, Patrick M. Navolanic, M. Worth Calfee, Martin McMahon and Everett C. Pesci and has published in prestigious journals such as Cancer Research, Oncogene and Infection and Immunity.

In The Last Decade

John G. Shelton

17 papers receiving 923 citations

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
John G. Shelton United States 14 638 267 105 102 85 17 929
Yumiko Hirokawa Australia 19 528 0.8× 271 1.0× 68 0.6× 61 0.6× 51 0.6× 31 910
Barry J. Maurer United States 17 1.0k 1.6× 164 0.6× 53 0.5× 151 1.5× 97 1.1× 40 1.3k
Michelle Wong United States 10 674 1.1× 181 0.7× 87 0.8× 85 0.8× 124 1.5× 18 973
Theoni Trangas Greece 19 717 1.1× 299 1.1× 98 0.9× 318 3.1× 72 0.8× 52 1.2k
Anna Stępczyńska Germany 7 769 1.2× 222 0.8× 53 0.5× 140 1.4× 156 1.8× 9 1.2k
Li-Yuan Bai Taiwan 17 466 0.7× 150 0.6× 52 0.5× 99 1.0× 102 1.2× 42 869
K. M. Nicholson United Kingdom 4 1.1k 1.8× 380 1.4× 141 1.3× 227 2.2× 112 1.3× 6 1.5k
Sen Zhang China 11 795 1.2× 161 0.6× 75 0.7× 83 0.8× 75 0.9× 24 1.0k
Xiaohong Yang China 17 610 1.0× 247 0.9× 71 0.7× 183 1.8× 119 1.4× 56 1.1k
Maria Assunta Bevilacqua Italy 18 503 0.8× 133 0.5× 65 0.6× 106 1.0× 71 0.8× 30 918

Countries citing papers authored by John G. Shelton

Since Specialization
Citations

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

Fields of papers citing papers by John G. Shelton

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by John G. Shelton. 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 John G. Shelton. The network helps show where John G. Shelton may publish in the future.

Co-authorship network of co-authors of John G. Shelton

This figure shows the co-authorship network connecting the top 25 collaborators of John G. Shelton. A scholar is included among the top collaborators of John G. Shelton 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 John G. Shelton. John G. Shelton 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.
Abrams, Stephen L., Linda S. Steelman, John G. Shelton, et al.. (2010). Enhancing therapeutic efficacy by targeting non-oncogene addicted cells with combinations of signal transduction inhibitors and chemotherapy. Cell Cycle. 9(9). 1839–1846. 21 indexed citations
2.
Steelman, Linda S., Stephen L. Abrams, John G. Shelton, et al.. (2010). Dominant roles of the Raf/MEK/ERK pathway in cell cycle progression, prevention of apoptosis and sensitivity to chemotherapeutic drugs. Cell Cycle. 9(8). 1629–1638. 33 indexed citations
3.
Abrams, Stephen L., Linda S. Steelman, John G. Shelton, et al.. (2010). The Raf/MEK/ERK pathway can govern drug resistance, apoptosis and sensitivity to targeted therapy. Cell Cycle. 9(9). 1781–1791. 103 indexed citations
4.
Shelton, John G., Linda S. Steelman, Steven L. Abrams, et al.. (2005). Effects of Endogenous Epidermal Growth Factor Receptor Signaling on DNA Synthesis and ERK Activation in a Cytokine-Dependent Hematopoietic Cell Line. Cell Cycle. 4(6). 818–821. 9 indexed citations
5.
Shelton, John G., Linda S. Steelman, Steven L. Abrams, et al.. (2005). Conditional EGFR Promotes Cell Cycle Progression and Prevention of Apoptosis in the Absence of Autocrine Cytokines. Cell Cycle. 4(6). 822–830. 23 indexed citations
6.
Konopleva, Marina, Yuexi Shi, Linda S. Steelman, et al.. (2005). Development of a Conditional In vivo Model to Evaluate the Efficacy of Small Molecule Inhibitors for the Treatment of Raf-Transformed Hematopoietic Cells. Cancer Research. 65(21). 9962–9970. 13 indexed citations
7.
Calfee, M. Worth, John G. Shelton, James A. McCubrey, & Everett C. Pesci. (2005). Solubility and Bioactivity of the Pseudomonas Quinolone Signal Are Increased by a Pseudomonas aeruginosa -Produced Surfactant. Infection and Immunity. 73(2). 878–882. 71 indexed citations
8.
Shelton, John G., Linda S. Steelman, Steve L. Abrams, et al.. (2005). The epidermal growth factor receptor gene family as a target for therapeutic intervention in numerous cancers: what’s genetics got to do with it?. Expert Opinion on Therapeutic Targets. 9(5). 1009–1030. 41 indexed citations
9.
McCubrey, James A., John G. Shelton, Linda S. Steelman, et al.. (2004). Effects of a conditionally active v-ErbB and an EGF-R inhibitor on transformation of NIH-3T3 cells and abrogation of cytokine dependency of hematopoietic cells. Oncogene. 23(47). 7810–7820. 12 indexed citations
10.
Akula, Shaw M., et al.. (2004). Raf promotes human herpesvirus-8 (HHV-8/KSHV) infection. Oncogene. 23(30). 5227–5241. 32 indexed citations
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Shelton, John G., Fumin Chang, John Tayu Lee, et al.. (2004). B-Raf and Insulin Synergistically Prevent Apoptosis and Induce Cell Cycle Progression in Hematopoietic Cell. Cell Cycle. 3(2). 184–191. 15 indexed citations
14.
Shelton, John G., Linda S. Steelman, John Tayu Lee, et al.. (2003). Effects of the RAF/MEK/ERK and PI3K/AKT signal transduction pathways on the abrogation of cytokine-dependence and prevention of apoptosis in hematopoietic cells. Oncogene. 22(16). 2478–2492. 78 indexed citations
15.
Chang, Fumin, Linda S. Steelman, John G. Shelton, et al.. (2003). Regulation of cell cycle progression and apoptosis by the Ras/Raf/MEK/ERK pathway (Review).. PubMed. 22(3). 469–80. 332 indexed citations
16.
Shelton, John G., et al.. (2001). Importance of the T cell receptor α-chain transmembrane distal region for assembly with cognate subunits. Molecular Immunology. 38(4). 259–265. 5 indexed citations
17.
McCubrey, James A., Linda S. Steelman, William L. Blalock, et al.. (2001). Synergistic effects of pi3k/akt on abrogation of cytokine-dependency induced by oncogenic raf. Advances in Enzyme Regulation. 41(1). 289–323. 20 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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