Jamie S. Mader

1.7k total citations
19 papers, 1.4k citations indexed

About

Jamie S. Mader is a scholar working on Immunology, Microbiology and Molecular Biology. According to data from OpenAlex, Jamie S. Mader has authored 19 papers receiving a total of 1.4k indexed citations (citations by other indexed papers that have themselves been cited), including 11 papers in Immunology, 8 papers in Microbiology and 7 papers in Molecular Biology. Recurrent topics in Jamie S. Mader's work include Antimicrobial Peptides and Activities (8 papers), Immunotherapy and Immune Responses (4 papers) and RNA Interference and Gene Delivery (3 papers). Jamie S. Mader is often cited by papers focused on Antimicrobial Peptides and Activities (8 papers), Immunotherapy and Immune Responses (4 papers) and RNA Interference and Gene Delivery (3 papers). Jamie S. Mader collaborates with scholars based in Canada and France. Jamie S. Mader's co-authors include David W. Hoskin, David Conrad, Suzanne J. Furlong, Jayme Salsman, Jonathan Blay, Robert E. W. Hancock, R. Chris Bleackley, Deniz Top, Roberto de Antueno and Roy Duncan and has published in prestigious journals such as The EMBO Journal, The Journal of Immunology and Cancer Research.

In The Last Decade

Jamie S. Mader

19 papers receiving 1.4k citations

Peers

Jamie S. Mader
Jin‐Long Yang United States
Rita J. Proske United States
Christopher J. Barker Sweden
Liane Mende‐Mueller United States
Antoinette Monod Switzerland
Ji‐Hyun Yeom South Korea
Su‐Jin Kang South Korea
Annick Pierce France
Elizabeth A. Ottinger United States
Amy A. Baxter Australia
Jin‐Long Yang United States
Jamie S. Mader
Citations per year, relative to Jamie S. Mader Jamie S. Mader (= 1×) peers Jin‐Long Yang

Countries citing papers authored by Jamie S. Mader

Since Specialization
Citations

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

Fields of papers citing papers by Jamie S. Mader

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Jamie S. Mader. 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 Jamie S. Mader. The network helps show where Jamie S. Mader may publish in the future.

Co-authorship network of co-authors of Jamie S. Mader

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

All Works

19 of 19 papers shown
1.
Mader, Jamie S., Catherine Ewen, Robert E. W. Hancock, & R. Chris Bleackley. (2011). The Human Cathelicidin, LL-37, Induces Granzyme-mediated Apoptosis in Regulatory T Cells. Journal of Immunotherapy. 34(3). 229–235. 39 indexed citations
2.
Furlong, Suzanne J., Jamie S. Mader, & David W. Hoskin. (2010). Bovine lactoferricin induces caspase-independent apoptosis in human B-lymphoma cells and extends the survival of immune-deficient mice bearing B-lymphoma xenografts. Experimental and Molecular Pathology. 88(3). 371–375. 50 indexed citations
3.
Mader, Jamie S., Marcelo Marcet‐Palacios, Robert E. W. Hancock, & R. Chris Bleackley. (2010). The human cathelicidin, LL-37, induces granzyme-mediated apoptosis in cytotoxic T lymphocytes. Experimental Cell Research. 317(4). 531–538. 23 indexed citations
4.
Mader, Jamie S., Neeloffer Mookherjee, Robert E. W. Hancock, & R. Chris Bleackley. (2009). The Human Host Defense Peptide LL-37 Induces Apoptosis in a Calpain- and Apoptosis-Inducing Factor–Dependent Manner Involving Bax Activity. Molecular Cancer Research. 7(5). 689–702. 67 indexed citations
5.
Hoskin, David W., Jamie S. Mader, Suzanne J. Furlong, David Conrad, & Jonathan Blay. (2008). Inhibition of T cell and natural killer cell function by adenosine and its contribution to immune evasion by tumor cells (Review). International Journal of Oncology. 32(3). 527–35. 201 indexed citations
6.
Conrad, David, Jamie S. Mader, Robert M. Boudreau, et al.. (2008). 2-Chloro-2'-deoxyadenosine-induced apoptosis in T leukemia cells is mediated via a caspase-3-dependent mitochondrial feedback amplification loop. International Journal of Oncology. 11 indexed citations
7.
Mader, Jamie S., Angela M. Richardson, Jayme Salsman, et al.. (2007). Bovine lactoferricin causes apoptosis in Jurkat T-leukemia cells by sequential permeabilization of the cell membrane and targeting of mitochondria. Experimental Cell Research. 313(12). 2634–2650. 89 indexed citations
8.
Mader, Jamie S., Daniel Smyth, Jean S. Marshall, & David W. Hoskin. (2006). Bovine Lactoferricin Inhibits Basic Fibroblast Growth Factor- and Vascular Endothelial Growth Factor165-Induced Angiogenesis by Competing for Heparin-Like Binding Sites on Endothelial Cells. American Journal Of Pathology. 169(5). 1753–1766. 60 indexed citations
9.
Mader, Jamie S. & David W. Hoskin. (2006). Cationic antimicrobial peptides as novel cytotoxic agents for cancer treatment. Expert Opinion on Investigational Drugs. 15(8). 933–946. 355 indexed citations
10.
Furlong, Suzanne J., Jamie S. Mader, & David W. Hoskin. (2006). Lactoferricin-induced apoptosis in estrogen-nonresponsive MDA-MB-435 breast cancer cells is enhanced by C6 ceramide or tamoxifen. Oncology Reports. 15(5). 1385–90. 60 indexed citations
11.
Mader, Jamie S. & David W. Hoskin. (2005). Lactoferricin, a peptide derived from bovine lactoferrin, has anti-angiogenic activity. Cancer Research. 65. 712–712. 1 indexed citations
12.
Top, Deniz, Roberto de Antueno, Jayme Salsman, et al.. (2005). Liposome reconstitution of a minimal protein‐mediated membrane fusion machine. The EMBO Journal. 24(17). 2980–2988. 48 indexed citations
13.
Mader, Jamie S., et al.. (2005). Adenosine-induced apoptosis in EL-4 thymoma cells is caspase-independent and mediated through a non-classical adenosine receptor. Experimental and Molecular Pathology. 79(3). 249–258. 25 indexed citations
14.
Mader, Jamie S., Jayme Salsman, David Conrad, & David W. Hoskin. (2005). Bovine lactoferricin selectively induces apoptosis in human leukemia and carcinoma cell lines. Molecular Cancer Therapeutics. 4(4). 612–624. 213 indexed citations
15.
Mader, Jamie S., et al.. (2005). Contribution of reactive oxygen species and caspase-3 to apoptosis and attenuated ICAM-1 expression by paclitaxel-treated MDA-MB-435 breast carcinoma cells.. PubMed. 27(6). 1717–26. 26 indexed citations
16.
Conrad, David, et al.. (2004). Ryanodine receptor signaling is required for anti‐CD3‐induced T cell proliferation, interleukin‐2 synthesis, and interleukin‐2 receptor signaling. Journal of Cellular Biochemistry. 92(2). 387–399. 26 indexed citations
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Butler, Jared, et al.. (2003). Adenosine inhibits activation‐induced T cell expression of CD2 and CD28 co‐stimulatory molecules: Role of interleukin‐2 and cyclic AMP signaling pathways. Journal of Cellular Biochemistry. 89(5). 975–991. 45 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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