James G. Cripps

1.3k total citations
10 papers, 1.0k citations indexed

About

James G. Cripps is a scholar working on Immunology, Molecular Biology and Oncology. According to data from OpenAlex, James G. Cripps has authored 10 papers receiving a total of 1.0k indexed citations (citations by other indexed papers that have themselves been cited), including 8 papers in Immunology, 4 papers in Molecular Biology and 3 papers in Oncology. Recurrent topics in James G. Cripps's work include Immune Cell Function and Interaction (4 papers), Cell death mechanisms and regulation (3 papers) and Immune Response and Inflammation (3 papers). James G. Cripps is often cited by papers focused on Immune Cell Function and Interaction (4 papers), Cell death mechanisms and regulation (3 papers) and Immune Response and Inflammation (3 papers). James G. Cripps collaborates with scholars based in United States, United Kingdom and Brazil. James G. Cripps's co-authors include James D. Gorham, Giovanni Quarato, Ricardo Weinlich, Douglas R. Green, Diego A. Rodríguez, Christopher P. Dillon, Thirumala‐Devi Kanneganti, Prajwal Gurung, Katherine Verbist and Fabien Llambi and has published in prestigious journals such as Cell, The Journal of Immunology and Hepatology.

In The Last Decade

James G. Cripps

10 papers receiving 1.0k citations

Peers

James G. Cripps

MB

IMMUN

ONCOL

EPIDE

CR

Tehila Ben-Moshe Israel

Hirotaka Kazama Japan

Hirokazu Hirata Japan

Viera Kasparcova United States

Adnan K. Mookhtiar United States

Kiichi Murakami Canada

Lauren Dare United States

Bernd Matiba Germany

Eva Källberg Sweden

Leal Oburoglu Sweden

Tehila Ben-Moshe Israel

James G. Cripps

569 ×0.8

MB

361 ×0.6

IMMUN

142 ×1.1

ONCOL

136 ×1.2

EPIDE

104 ×1.0

CR

Citations per year, relative to James G. Cripps James G. Cripps (= 1×) peers Tehila Ben-Moshe

Countries citing papers authored by James G. Cripps

Since Specialization

Citations

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

Fields of papers citing papers by James G. Cripps

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of James G. Cripps

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

All Works

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10 of 10 papers shown

1.

Rodríguez, Diego A., Bart Tummers, Jeremy J.P. Shaw, et al.. (2024). The interaction between RIPK1 and FADD controls perinatal lethality and inflammation. Cell Reports. 43(6). 114335–114335. 5 indexed citations

2.

Rodríguez, Diego A., Ricardo Weinlich, S. M. Brown, et al.. (2015). Characterization of RIPK3-mediated phosphorylation of the activation loop of MLKL during necroptosis. Cell Death and Differentiation. 23(1). 76–88. 294 indexed citations

3.

Dillon, Christopher P., Ricardo Weinlich, Diego A. Rodríguez, et al.. (2014). RIPK1 Blocks Early Postnatal Lethality Mediated by Caspase-8 and RIPK3. Cell. 157(5). 1189–1202. 429 indexed citations

4.

Cripps, James G., et al.. (2012). Liver inflammation in a mouse model of Th1 hepatitis despite the absence of invariant NKT cells or the Th1 chemokine receptors CXCR3 and CCR5. Laboratory Investigation. 92(10). 1461–1471. 5 indexed citations

5.

Cripps, James G. & James D. Gorham. (2011). MDSC in autoimmunity. International Immunopharmacology. 11(7). 789–793. 116 indexed citations

6.

Cripps, James G., et al.. (2010). Type 1 T Helper Cells Induce the Accumulation of Myeloid-Derived Suppressor Cells in the Inflamed Tgfb1 Knockout Mouse Liver. Hepatology. 52(4). 1350–1359. 77 indexed citations

7.

Milks, M. Wesley, James G. Cripps, Heping Lin, et al.. (2009). The role of Ifng in alterations in liver gene expression in a mouse model of fulminant autoimmune hepatitis. Liver International. 29(9). 1307–1315. 10 indexed citations

8.

Robinson, Richard, et al.. (2009). End-Organ Damage in a Mouse Model of Fulminant Liver Inflammation Requires CD4+ T Cell Production of IFN-γ but Is Independent of Fas. The Journal of Immunology. 182(5). 3278–3284. 30 indexed citations

9.

Sun, Xichun, et al.. (2006). The immunoregulatory effects of gangliosides involve immune deviation favoring type-2 T cell responses. Journal of Leukocyte Biology. 79(3). 586–595. 25 indexed citations

10.

Cripps, James G., et al.. (2005). Modulation of acute inflammation by targeting glycosaminoglycan–cytokine interactions. International Immunopharmacology. 5(11). 1622–1632. 23 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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