John C. Scatizzi

749 total citations
16 papers, 610 citations indexed

About

John C. Scatizzi is a scholar working on Immunology, Molecular Biology and Rheumatology. According to data from OpenAlex, John C. Scatizzi has authored 16 papers receiving a total of 610 indexed citations (citations by other indexed papers that have themselves been cited), including 13 papers in Immunology, 7 papers in Molecular Biology and 5 papers in Rheumatology. Recurrent topics in John C. Scatizzi's work include Cell death mechanisms and regulation (5 papers), Phagocytosis and Immune Regulation (5 papers) and Systemic Lupus Erythematosus Research (4 papers). John C. Scatizzi is often cited by papers focused on Cell death mechanisms and regulation (5 papers), Phagocytosis and Immune Regulation (5 papers) and Systemic Lupus Erythematosus Research (4 papers). John C. Scatizzi collaborates with scholars based in United States, Belgium and Australia. John C. Scatizzi's co-authors include Harris Perlman, Jack Hutcheson, G. Kenneth Haines, Laurie S. Davis, Quan‐Zhen Li, Chandra Mohan, Tianfu Wu, G. Kenneth Haines, Akbar M. Siddiqui and Dwight H. Kono and has published in prestigious journals such as The Journal of Experimental Medicine, Immunity and The Journal of Immunology.

In The Last Decade

John C. Scatizzi

15 papers receiving 599 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 C. Scatizzi United States 14 391 256 131 112 60 16 610
S. M. Shahjahan Miah United States 18 393 1.0× 267 1.0× 70 0.5× 128 1.1× 61 1.0× 23 665
J D Mountz United States 12 448 1.1× 210 0.8× 165 1.3× 96 0.9× 49 0.8× 14 676
Noriyasu Seki Japan 13 407 1.0× 206 0.8× 113 0.9× 163 1.5× 36 0.6× 26 693
Changchuin Mao United States 11 303 0.8× 217 0.8× 71 0.5× 165 1.5× 49 0.8× 20 573
David Plows Greece 8 186 0.5× 159 0.6× 189 1.4× 141 1.3× 81 1.4× 9 504
Michaela Seeling Germany 11 384 1.0× 343 1.3× 117 0.9× 65 0.6× 23 0.4× 17 683
Tammy P. Cheng United States 12 284 0.7× 135 0.5× 63 0.5× 111 1.0× 36 0.6× 12 521
J L Chu United States 7 376 1.0× 203 0.8× 153 1.2× 40 0.4× 44 0.7× 10 525
Yujun Sheng China 15 437 1.1× 165 0.6× 252 1.9× 79 0.7× 40 0.7× 56 724
Inna Verbovetski Israel 12 456 1.2× 201 0.8× 61 0.5× 55 0.5× 26 0.4× 13 647

Countries citing papers authored by John C. Scatizzi

Since Specialization
Citations

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

Fields of papers citing papers by John C. Scatizzi

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of John C. Scatizzi

This figure shows the co-authorship network connecting the top 25 collaborators of John C. Scatizzi. A scholar is included among the top collaborators of John C. Scatizzi 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 C. Scatizzi. John C. Scatizzi 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.
Maine, Christian J., Kristi Marquardt, John C. Scatizzi, et al.. (2014). The effect of the autoimmunity-associated gene, PTPN22, on a BXSB-derived model of lupus. Clinical Immunology. 156(1). 65–73. 14 indexed citations
2.
Koh, Yi Ting, John C. Scatizzi, Brian R. Lawson, et al.. (2013). Role of Nucleic Acid–Sensing TLRs in Diverse Autoantibody Specificities and Anti-Nuclear Antibody–Producing B Cells. The Journal of Immunology. 190(10). 4982–4990. 38 indexed citations
3.
Scatizzi, John C., et al.. (2012). The Lbw2 Locus Promotes Autoimmune Hemolytic Anemia. The Journal of Immunology. 188(7). 3307–3314. 8 indexed citations
4.
González‐Quintial, Rosana, Brian R. Lawson, John C. Scatizzi, et al.. (2011). Systemic Autoimmunity and Lymphoproliferation Are Associated with Excess IL-7 and Inhibited by IL-7Rα Blockade. PLoS ONE. 6(11). e27528–e27528. 36 indexed citations
5.
Scatizzi, John C., Jack Hutcheson, Richard M. Pope, et al.. (2010). Bim–Bcl‐2 homology 3 mimetic therapy is effective at suppressing inflammatory arthritis through the activation of myeloid cell apoptosis. Arthritis & Rheumatism. 62(2). 441–451. 37 indexed citations
6.
Scatizzi, John C., Melissa Mavers, Jack Hutcheson, et al.. (2009). The CDK domain of p21 is a suppressor of IL‐1β‐mediated inflammation in activated macrophages. European Journal of Immunology. 39(3). 820–825. 58 indexed citations
7.
Hutcheson, Jack, John C. Scatizzi, Akbar M. Siddiqui, et al.. (2008). Combined Deficiency of Proapoptotic Regulators Bim and Fas Results in the Early Onset of Systemic Autoimmunity. Immunity. 28(2). 206–217. 170 indexed citations
8.
Scatizzi, John C., et al.. (2007). Pro-apoptotic Bid is required for the resolution of the effector phase of inflammatory arthritis. Arthritis Research & Therapy. 9(3). R49–R49. 35 indexed citations
9.
Scatizzi, John C., et al.. (2006). Bim deficiency leads to exacerbation and prolongation of joint inflammation in experimental arthritis. Arthritis & Rheumatism. 54(10). 3182–3193. 44 indexed citations
10.
Scatizzi, John C., Jack Hutcheson, James M. Woods, et al.. (2006). p21Cip1 Is Required for the Development of Monocytes and Their Response to Serum Transfer-induced Arthritis. American Journal Of Pathology. 168(5). 1531–1541. 28 indexed citations
11.
Woods, James M., et al.. (2006). A cell-cycle independent role for p21 in regulating synovial fibroblast migration in rheumatoid arthritis. Arthritis Research & Therapy. 8(4). R113–R113. 18 indexed citations
12.
Brown, Nathaniel J., Jack Hutcheson, John C. Scatizzi, et al.. (2005). Fas Death Receptor Signaling Represses Monocyte Numbers and Macrophage Activation In Vivo.. The Journal of Immunology. 174(6). 3818–3818. 2 indexed citations
13.
Hutcheson, Jack, John C. Scatizzi, Nathaniel J. Brown, et al.. (2005). Combined loss of proapoptotic genes Bak or Bax with Bim synergizes to cause defects in hematopoiesis and in thymocyte apoptosis. The Journal of Experimental Medicine. 201(12). 1949–1960. 44 indexed citations
14.
Brown, Nathaniel J., Jack Hutcheson, John C. Scatizzi, et al.. (2004). Fas Death Receptor Signaling Represses Monocyte Numbers and Macrophage Activation In Vivo. The Journal of Immunology. 173(12). 7584–7593. 36 indexed citations
15.
Scatizzi, John C., Stefano Fiore, Alisa E. Koch, et al.. (2004). Retinoblastoma suppression of matrix metalloproteinase 1, but not interleukin‐6, through a p38‐dependent pathway in rheumatoid arthritis synovial fibroblasts. Arthritis & Rheumatism. 50(1). 78–87. 20 indexed citations
16.
Scatizzi, John C., et al.. (2004). IL-4 and IL-10 Inhibition of Spontaneous Monocyte Apoptosis Is Associated with Flip Upregulation. Inflammation. 28(3). 139–145. 22 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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