Jane K. Relton

5.8k total citations · 1 hit paper
38 papers, 4.8k citations indexed

About

Jane K. Relton is a scholar working on Neurology, Cellular and Molecular Neuroscience and Molecular Biology. According to data from OpenAlex, Jane K. Relton has authored 38 papers receiving a total of 4.8k indexed citations (citations by other indexed papers that have themselves been cited), including 16 papers in Neurology, 14 papers in Cellular and Molecular Neuroscience and 11 papers in Molecular Biology. Recurrent topics in Jane K. Relton's work include Neuroinflammation and Neurodegeneration Mechanisms (13 papers), Nerve injury and regeneration (8 papers) and Stress Responses and Cortisol (6 papers). Jane K. Relton is often cited by papers focused on Neuroinflammation and Neurodegeneration Mechanisms (13 papers), Nerve injury and regeneration (8 papers) and Stress Responses and Cortisol (6 papers). Jane K. Relton collaborates with scholars based in United States, United Kingdom and Russia. Jane K. Relton's co-authors include Nancy J. Rothwell, Lisa E. Goehler, Linda R. Watkins, Nicole Tartaglia, David Martin, Steven F. Maier, Nancy J. Rothwell, Benxiu Ji, Steven F. Maier and Julio Herrero García and has published in prestigious journals such as The Journal of Experimental Medicine, Journal of Neuroscience and Nature Neuroscience.

In The Last Decade

Jane K. Relton

38 papers receiving 4.7k citations

Hit Papers

LINGO-1 is a component of the Nogo-66 receptor/p75 signal... 2004 2026 2011 2018 2004 200 400 600

Peers

Jane K. Relton
Jane K. Relton
Citations per year, relative to Jane K. Relton Jane K. Relton (= 1×) peers Bernardo Castellano

Countries citing papers authored by Jane K. Relton

Since Specialization
Citations

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

Fields of papers citing papers by Jane K. Relton

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Jane K. Relton. 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 Jane K. Relton. The network helps show where Jane K. Relton may publish in the future.

Co-authorship network of co-authors of Jane K. Relton

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

All Works

20 of 20 papers shown
1.
Campbell, Sandra J., Ute‐Christiane Meier, Yanyan Jiang, et al.. (2010). Sickness behaviour is induced by a peripheral CXC-chemokine also expressed in Multiple Sclerosis and EAE. Brain Behavior and Immunity. 24(5). 738–746. 41 indexed citations
2.
Trabold, Raimund, Klaus Zweckberger, Jane K. Relton, et al.. (2009). The Role of Bradykinin B1 and B2 Receptors for Secondary Brain Damage after Traumatic Brain Injury in Mice. Journal of Cerebral Blood Flow & Metabolism. 30(1). 130–139. 61 indexed citations
3.
Ji, Benxiu, Lauren C. Case, Kai Liu, et al.. (2008). Assessment of functional recovery and axonal sprouting in oligodendrocyte-myelin glycoprotein (OMgp) null mice after spinal cord injury. Molecular and Cellular Neuroscience. 39(2). 258–267. 48 indexed citations
4.
Fleming, Jennifer C., et al.. (2008). α4β1 integrin blockade after spinal cord injury decreases damage and improves neurological function. Experimental Neurology. 214(2). 147–159. 54 indexed citations
5.
Watson, Paul, Martin J. Humphries, Jane K. Relton, et al.. (2006). Integrin-binding RGD peptides induce rapid intracellular calcium increases and MAPK signaling in cortical neurons. Molecular and Cellular Neuroscience. 34(2). 147–154. 31 indexed citations
6.
Ji, Benxiu, Mingwei Li, Wutian Wu, et al.. (2006). LINGO-1 antagonist promotes functional recovery and axonal sprouting after spinal cord injury. Molecular and Cellular Neuroscience. 33(3). 311–320. 122 indexed citations
7.
Ji, Benxiu, Mingwei Li, Stéphane Budel, et al.. (2005). Effect of combined treatment with methylprednisolone and soluble Nogo‐66 receptor after rat spinal cord injury. European Journal of Neuroscience. 22(3). 587–594. 46 indexed citations
8.
Mi, Sha, Xinhua Lee, Zhaohui Shao, et al.. (2004). LINGO-1 is a component of the Nogo-66 receptor/p75 signaling complex. Nature Neuroscience. 7(3). 221–228. 660 indexed citations breakdown →
9.
Relton, Jane K., et al.. (1996). Peripheral Administration of Interleukin-1 Receptor Antagonist Inhibits Brain Damage after Focal Cerebral Ischemia in the Rat. Experimental Neurology. 138(2). 206–213. 176 indexed citations
10.
Watkins, L.R., Lisa E. Goehler, Jane K. Relton, et al.. (1995). Blockade of interleukin-1 induced hyperthermia by subdiaphragmatic vagotomy: evidence for vagal mediation of immune-brain communication. Neuroscience Letters. 183(1-2). 27–31. 417 indexed citations
11.
12.
Watkins, Linda R., Lisa E. Goehler, Jane K. Relton, Michael Brewer, & Steven F. Maier. (1995). Mechanisms of tumor necrosis factor-α (TNF-α) hyperalgesia. Brain Research. 692(1-2). 244–250. 177 indexed citations
13.
Fleshner, Monika, et al.. (1995). Interleukin-1β induced corticosterone elevation and hypothalamic NE depletion is vagally mediated. Brain Research Bulletin. 37(6). 605–610. 155 indexed citations
14.
Strijbos, Paul J. L. M., Jane K. Relton, & Nancy J. Rothwell. (1994). Corticotrophin-releasing factor antagonist inhibits neuronal damage induced by focal cerebral ischaemia or activation of NMDA receptors in the rat brain. Brain Research. 656(2). 405–408. 78 indexed citations
15.
Relton, Jane K., Paul J. L. M. Strijbos, A. L. Cooper, & Nancy J. Rothwell. (1993). Dietary N-3 fatty acids inhibit ischaemic and excitotoxic brain damage in the rat. Brain Research Bulletin. 32(3). 223–226. 32 indexed citations
16.
Rothwell, Nancy J. & Jane K. Relton. (1993). Involvement of cytokines in acute neurodegeneration in the CNS. Neuroscience & Biobehavioral Reviews. 17(2). 217–227. 140 indexed citations
17.
Relton, Jane K. & Nancy J. Rothwell. (1992). Interleukin-1 receptor antagonist inhibits ischaemic and excitotoxic neuronal damage in the rat. Brain Research Bulletin. 29(2). 243–246. 465 indexed citations
18.
Relton, Jane K.. (1992). Interleukin receptor antagonist inhibits neuronal damage induced by cerebral ischemia or NMDA-receptor activation in the rat. Brain Research Bulletin. 585. 135–141. 7 indexed citations
19.
Black, Mark D., F. Carey, A.R. Crossman, Jane K. Relton, & Nancy J. Rothwell. (1992). Lipocortin-1 inhibits NMDA receptor-mediated neuronal damage in the striatum of the rat. Brain Research. 585(1-2). 135–140. 49 indexed citations
20.
Relton, Jane K., Paul J. L. M. Strijbos, C.T. O'Shaughnessy, et al.. (1991). Lipocortin-1 is an endogenous inhibitor of ischemic damage in the rat brain.. The Journal of Experimental Medicine. 174(2). 305–310. 120 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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