Johan Heldin

630 citations
23 papers · 505 · h-index 12

Impact in

  • Cell Biology top 10%
    • Proteoglycans and glycosaminoglycans research
    • Biotin and Related Studies
    • MicroRNA in disease regulation

Papers in

    • Cellular transport and secretion 3
    • Caveolin-1 and cellular processes 2
    • Carcinogens and Genotoxicity Assessment 2

Johan Heldin

21 papers receiving 493 citations

Peers

Johan Heldin
Comparison fields: 5 of 67
  • Cell Biology 81
  • Cancer Research 61
  • Molecular Biology 246
  • Endocrine and Autonomic Systems 18
  • Cellular and Molecular Neuroscience 46
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Citations per field
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Citations per year

Countries citing papers authored by Johan Heldin

Since Specialization
Citations

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

Fields of papers citing papers by Johan Heldin

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Johan Heldin. 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 Johan Heldin. The network helps show where Johan Heldin may publish in the future.

Co-authors

The 25 scholars most cited alongside Johan Heldin, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.

Border = papers with Johan Heldin Line = papers co-authored together Johan Heldin links everyone, so they are left out of the graph.

All Works

20 of 20 papers shown

Showing the 20 most-cited of 23 papers — load more, or switch the sort, to bring in the rest.

#Work
1 201598
2 200982
3 201255
4 201344
5 201842
6 201128
7 201724
8 201724
9 201719
10 201218
11 202213
12 202212
13 201911
14 202310
15 20249
16 20195
17 20235
18 20242
19 20242
20 20211

About Johan Heldin

Johan Heldin is a scholar working on Cell Biology, Cancer Research, Molecular Biology, Biophysics and Cellular and Molecular Neuroscience, having authored 23 papers that have together received 505 indexed citations. Recurring topics across this work include Advanced biosensing and bioanalysis techniques (6 papers), Protein Kinase Regulation and GTPase Signaling (4 papers), Cellular transport and secretion (3 papers), Caveolin-1 and cellular processes (2 papers), Carcinogens and Genotoxicity Assessment (2 papers), Neuropeptides and Animal Physiology (2 papers), TGF-β signaling in diseases (2 papers) and Angiogenesis and VEGF in Cancer (2 papers). The work is most often cited by research in Cell Biology (81 citations), Cancer Research (61 citations), Molecular Biology (246 citations), Endocrine and Autonomic Systems (18 citations) and Cellular and Molecular Neuroscience (46 citations). Johan Heldin has collaborated with scholars based in Sweden, Germany and United States. Frequent co-authors include Ola Söderberg, Johan Kreuger, Peder Fredlund Fuchs, Tomas Larsson, Bo Xu, Dan Larhammar, Görel Sundström, Irmeli Barkefors, Björn Koos and Karin Grannas. Their work appears in journals such as Nature Communications, Nucleic Acids Research, Biochemical and Biophysical Research Communications, Cellular Signalling and Experimental Cell Research.

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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