Bryce G. Johnson

1.4k total citations
15 papers, 1.1k citations indexed

About

Bryce G. Johnson is a scholar working on Molecular Biology, Immunology and Nephrology. According to data from OpenAlex, Bryce G. Johnson has authored 15 papers receiving a total of 1.1k indexed citations (citations by other indexed papers that have themselves been cited), including 10 papers in Molecular Biology, 4 papers in Immunology and 3 papers in Nephrology. Recurrent topics in Bryce G. Johnson's work include Renal and related cancers (4 papers), Biomarkers in Disease Mechanisms (2 papers) and Endoplasmic Reticulum Stress and Disease (2 papers). Bryce G. Johnson is often cited by papers focused on Renal and related cancers (4 papers), Biomarkers in Disease Mechanisms (2 papers) and Endoplasmic Reticulum Stress and Disease (2 papers). Bryce G. Johnson collaborates with scholars based in United States, Switzerland and China. Bryce G. Johnson's co-authors include Jeremy S. Duffield, Ivan G. Gomez, Shuyu Ren, Allie M. Roach, Naoki Nakagawa, Irina A. Leaf, Gamze Karaca, Jonathan Himmelfarb, Shiguang Liu and Cuiyan Xin and has published in prestigious journals such as Proceedings of the National Academy of Sciences, Journal of Clinical Investigation and Nature Communications.

In The Last Decade

Bryce G. Johnson

14 papers receiving 1.0k citations

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
Bryce G. Johnson United States 12 579 265 204 167 144 15 1.1k
Ivan G. Gomez United States 17 670 1.2× 292 1.1× 326 1.6× 164 1.0× 196 1.4× 26 1.3k
Xiaohe Cai United States 14 356 0.6× 336 1.3× 186 0.9× 154 0.9× 118 0.8× 24 1000
Xingbo Xu Germany 20 810 1.4× 168 0.6× 200 1.0× 203 1.2× 111 0.8× 46 1.4k
Ayano Kondo United States 8 1.0k 1.8× 224 0.8× 255 1.3× 152 0.9× 224 1.6× 15 1.6k
Brent M. Steer Canada 14 782 1.4× 269 1.0× 283 1.4× 196 1.2× 125 0.9× 21 1.4k
Cristina López-Blau Spain 4 451 0.8× 225 0.8× 98 0.5× 122 0.7× 61 0.4× 5 766
Madalina V. Nastase Germany 9 466 0.8× 114 0.4× 166 0.8× 127 0.8× 251 1.7× 12 1.1k
Arnaud Marlier United States 19 453 0.8× 337 1.3× 52 0.3× 122 0.7× 121 0.8× 26 930
Fumiaki Nogaki Japan 16 358 0.6× 174 0.7× 111 0.5× 77 0.5× 219 1.5× 39 951

Countries citing papers authored by Bryce G. Johnson

Since Specialization
Citations

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

Fields of papers citing papers by Bryce G. Johnson

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Bryce G. Johnson

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

All Works

15 of 15 papers shown
1.
Kim, Yeawon, Chuang Li, Chenjian Gu, et al.. (2023). MANF stimulates autophagy and restores mitochondrial homeostasis to treat autosomal dominant tubulointerstitial kidney disease in mice. Nature Communications. 14(1). 6493–6493. 30 indexed citations
2.
Ju, Wang, Agustin Casimiro‐Garcia, Bryce G. Johnson, et al.. (2023). A protein kinase C α and β inhibitor blunts hyperphagia to halt renal function decline and reduces adiposity in a rat model of obesity-driven type 2 diabetes. Scientific Reports. 13(1). 16919–16919.
3.
Marr, Elizabeth E., Thomas J. Mulhern, Michaela Welch, et al.. (2023). A platform to reproducibly evaluate human colon permeability and damage. Scientific Reports. 13(1). 8922–8922. 10 indexed citations
4.
Jelinsky, Scott A., Eric B. Bauman, Carla S. Veríssimo, et al.. (2022). Molecular and Functional Characterization of Human Intestinal Organoids and Monolayers for Modeling Epithelial Barrier. Inflammatory Bowel Diseases. 29(2). 195–206. 35 indexed citations
5.
Kim, Yeawon, Zheyu Wang, Chuang Li, et al.. (2021). Ultrabright plasmonic fluor nanolabel-enabled detection of a urinary ER stress biomarker in autosomal dominant tubulointerstitial kidney disease. American Journal of Physiology-Renal Physiology. 321(2). F236–F244. 6 indexed citations
6.
Lemos, Darío R., Gamze Karaca, Julia Wilflingseder, et al.. (2018). Interleukin-1β Activates a MYC-Dependent Metabolic Switch in Kidney Stromal Cells Necessary for Progressive Tubulointerstitial Fibrosis. Journal of the American Society of Nephrology. 29(6). 1690–1705. 166 indexed citations
7.
Dang, Lan, Takahide Aburatani, Graham Marsh, et al.. (2017). Hyperactive FOXO1 results in lack of tip stalk identity and deficient microvascular regeneration during kidney injury. Biomaterials. 141. 314–329. 24 indexed citations
8.
Johnson, Bryce G., Lan Dang, Graham Marsh, et al.. (2017). Uromodulin p.Cys147Trp mutation drives kidney disease by activating ER stress and apoptosis. Journal of Clinical Investigation. 127(11). 3954–3969. 46 indexed citations
9.
Dower, Ken, Shanrong Zhao, Franklin Schlerman, et al.. (2017). High resolution molecular and histological analysis of renal disease progression in ZSF1 fa/faCP rats, a model of type 2 diabetic nephropathy. PLoS ONE. 12(7). e0181861–e0181861. 13 indexed citations
10.
Johnson, Bryce G., Shuyu Ren, Gamze Karaca, et al.. (2017). Connective Tissue Growth Factor Domain 4 Amplifies Fibrotic Kidney Disease through Activation of LDL Receptor–Related Protein 6. Journal of the American Society of Nephrology. 28(6). 1769–1782. 34 indexed citations
11.
Nakagawa, Naoki, Luke Barron, Ivan G. Gomez, et al.. (2016). Pentraxin-2 suppresses c-Jun/AP-1 signaling to inhibit progressive fibrotic disease. JCI Insight. 1(20). e87446–e87446. 52 indexed citations
12.
Leaf, Irina A., Shunsaku Nakagawa, Bryce G. Johnson, et al.. (2016). Pericyte MyD88 and IRAK4 control inflammatory and fibrotic responses to tissue injury. Journal of Clinical Investigation. 127(1). 321–334. 119 indexed citations
13.
Gomez, Ivan G., Allie M. Roach, Naoki Nakagawa, et al.. (2016). TWEAK-Fn14 Signaling Activates Myofibroblasts to Drive Progression of Fibrotic Kidney Disease. Journal of the American Society of Nephrology. 27(12). 3639–3652. 36 indexed citations
14.
Gomez, Ivan G., Deidre A. MacKenna, Bryce G. Johnson, et al.. (2014). Anti–microRNA-21 oligonucleotides prevent Alport nephropathy progression by stimulating metabolic pathways. Journal of Clinical Investigation. 125(1). 141–156. 319 indexed citations
15.
Ren, Shuyu, Bryce G. Johnson, Yujiro Kida, et al.. (2013). LRP-6 is a coreceptor for multiple fibrogenic signaling pathways in pericytes and myofibroblasts that are inhibited by DKK-1. Proceedings of the National Academy of Sciences. 110(4). 1440–1445. 167 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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