Paul Säftig
Impact in
- Physiology top 0.02%
- Alzheimer's disease research and treatments
- Lysosomal Storage Disorders Research
- Calcium signaling and nucleotide metabolism
- Immunology and Allergy top 0.05%
- Cell Adhesion Molecules Research
Papers in
- Physiology 134
- Lysosomal Storage Disorders Research 77
- Alzheimer's disease research and treatments 51
- Calcium signaling and nucleotide metabolism 39
- Co-authors
- Eeva‐Liisa Eskelinen (21 shared papers)Bart De Strooper (35 shared papers)Karina Reiß (28 shared papers)Dieter Hartmann (38 shared papers)Kurt Von Figura (35 shared papers)Judith Klumperman (3 shared papers)Wim Annaert (12 shared papers)Katleen Craessaerts (8 shared papers)
- Journals
- Journal of Biological Chemistry (29 papers)Proceedings of the National Academy of Sciences (13 papers)Journal of Cell Science (11 papers)Journal of Neuroscience (10 papers)The EMBO Journal (8 papers)
- Partner nations
- GermanyUnited StatesBelgium
In The Last Decade
Paul Säftig
331 papers receiving 39.1k citations
Paul Säftig's Hit Papers
Peers
Comparison fields: 5 of 163
- Physiology 2.6k
- Immunology and Allergy 2.9k
- Cell Biology 7.6k
- Physiology 11.2k
- Cancer Research 3.7k
Countries citing papers authored by Paul Säftig
This map shows the geographic impact of Paul Säftig'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 Paul Säftig with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Paul Säftig more than expected).
Fields of papers citing papers by Paul Säftig
This network shows the impact of papers produced by Paul Säftig. 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 Paul Säftig. The network helps show where Paul Säftig may publish in the future.
Co-authors
The 25 scholars most cited alongside Paul Säftig, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.
All Works
Showing the 20 most-cited of 335 papers — load more, or switch the sort, to bring in the rest.
| # | Work | ||
|---|---|---|---|
| 1 | A presenilin-1-dependent γ-secretase-like protease mediates release of Notch intracellular domain Hit paper breakdown → | 1999 | 1722 |
| 2 | Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein Hit paper breakdown → | 1998 | 1483 |
| 3 | Lysosome biogenesis and lysosomal membrane proteins: trafficking meets function Hit paper breakdown → | 2009 | 1344 |
| 4 | Distinct roles for ADAM10 and ADAM17 in ectodomain shedding of six EGFR ligands Hit paper breakdown → | 2004 | 815 |
| 5 | The Tetraspanin CD63 Regulates ESCRT-Independent and -Dependent Endosomal Sorting during Melanogenesis Hit paper breakdown → | 2011 | 759 |
| 6 | Accumulation of autophagic vacuoles and cardiomyopathy in LAMP-2-deficient mice Hit paper breakdown → | 2000 | 745 |
| 7 | Role for Rab7 in maturation of late autophagic vacuoles Hit paper breakdown → | 2004 | 730 |
| 8 | Impaired osteoclastic bone resorption leads to osteopetrosis in cathepsin-K-deficient mice Hit paper breakdown → | 1998 | 716 |
| 9 | The disintegrin-like metalloproteinase ADAM10 is involved in constitutive cleavage of CX3CL1 (fractalkine) and regulates CX3CL1-mediated cell-cell adhesion Hit paper breakdown → | 2003 | 594 |
| 10 | Autophagy: A lysosomal degradation pathway with a central role in health and disease Hit paper breakdown → | 2008 | 589 |
| 11 | ADAM10 mediates E-cadherin shedding and regulates epithelial cell-cell adhesion, migration, and β-catenin translocation Hit paper breakdown → | 2005 | 541 |
| 12 | At the acidic edge: emerging functions for lysosomal membrane proteins Hit paper breakdown → | 2003 | 532 |
| 13 | Control of Peripheral Nerve Myelination by the ß-Secretase BACE1 Hit paper breakdown → | 2006 | 530 |
| 14 | LAMP proteins are required for fusion of lysosomes with phagosomes Hit paper breakdown → | 2007 | 527 |
| 15 | 2008 | 470 | |
| 16 | 1998 | 457 | |
| 17 | 2010 | 435 | |
| 18 | 2005 | 431 | |
| 19 | 2007 | 423 | |
| 20 | 1999 | 415 |
About Paul Säftig
Paul Säftig is a scholar working on Molecular Biology, Physiology, Cell Biology, Oncology and Immunology and Allergy, having authored 335 papers that have together received 39.6k indexed citations. Recurring topics across this work include Lysosomal Storage Disorders Research (77 papers), Cellular transport and secretion (67 papers), Alzheimer's disease research and treatments (51 papers), Cell Adhesion Molecules Research (45 papers), Calcium signaling and nucleotide metabolism (39 papers), Autophagy in Disease and Therapy (34 papers), Protease and Inhibitor Mechanisms (23 papers) and Peptidase Inhibition and Analysis (20 papers). The work is most often cited by research in Physiology (2.6k citations), Immunology and Allergy (2.9k citations), Cell Biology (7.6k citations), Physiology (11.2k citations) and Cancer Research (3.7k citations). Paul Säftig has collaborated with scholars based in Germany, United States and Belgium. Frequent co-authors include Eeva‐Liisa Eskelinen, Bart De Strooper, Karina Reiß, Dieter Hartmann, Kurt Von Figura, Judith Klumperman, Wim Annaert, Katleen Craessaerts, Andreas Ludwig and Carl Blobel. Their work appears in journals such as Journal of Biological Chemistry, Proceedings of the National Academy of Sciences, Journal of Cell Science, Journal of Neuroscience and The EMBO Journal.
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.