Joseph G. Naglich

1.9k citations
26 papers · 1.3k indexed · h-index 17
Topics
Cell death mechanisms and regulation (6 papers)Cancer, Hypoxia, and Metabolism (4 papers)Toxin Mechanisms and Immunotoxins (4 papers)

In The Last Decade

Joseph G. Naglich

26 papers receiving 1.3k citations

Peers

Joseph G. Naglich
Comparison fields: 5 of 87
  • Molecular Biology 757
  • Cancer Research 358
  • Immunology 344
  • Oncology 216
  • Biotechnology 154
Replace Gary S. Coombs with:
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Citations per field
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Citations per year

Countries citing papers authored by Joseph G. Naglich

Since Specialization
Citations

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

Fields of papers citing papers by Joseph G. Naglich

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Joseph G. Naglich

This figure shows the co-authorship network connecting the top 25 collaborators of Joseph G. Naglich. A scholar is included among the top collaborators of Joseph G. Naglich 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 Joseph G. Naglich. Joseph G. Naglich 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
#WorkIndexed citations
1 2
2 2
3 1
4 6
5 6
6 3
7 62
8 27
9 29
10 18
11 36
12 108
13
Cloning and characterization of a mouse gene with homology to the human von Hippel-Lindau disease tumor suppressor gene: implications for the potential organization of the human von Hippel-Lindau disease gene.
49
14
Germline mutations in the VHL tumor suppresssor gene are similar to somatic VHL aberrations in sporadic renal cell carcinoma
1
15 440
16 16
17 44
18 16
19 55
20 27

About Joseph G. Naglich

Joseph G. Naglich is a scholar working on Toxicology, Biotechnology and Cancer Research, having authored 26 papers that have together received 1.3k indexed citations. Recurring topics across this work include Cell death mechanisms and regulation (6 papers), Cancer, Hypoxia, and Metabolism (4 papers) and Toxin Mechanisms and Immunotoxins (4 papers). The work is most often cited by research in Cancer Research (358 citations), Biotechnology (154 citations) and Immunology (344 citations). Joseph G. Naglich has collaborated with scholars based in United States, Germany and Sweden. Frequent co-authors include Leon Eidels, David W. Russell, James E. Metherall, Jean M. Whaley, Ian Alan Holder, Robert E. Andrews, Bernd R. Seizinger, Nikolai Kley, Lawrence M. Gelbert and Hartmut P.H. Neumann. Their work appears in journals such as Cell, Proceedings of the National Academy of Sciences and Nature Communications.

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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