Matthew S. Eckman
Impact in
- Cell Biology top 5%
- Hippo pathway signaling and YAP/TAZ
- Cellular Mechanics and Interactions
- Microtubule and mitosis dynamics
- Neurology top 10%
- Neurofibromatosis and Schwannoma Cases
Papers in
-
- Microtubule and mitosis dynamics 1
- Cellular Mechanics and Interactions 1
- Oncology 2
- Cancer-related Molecular Pathways 1
- Co-authors
- Joseph L. Kissil (4 shared papers)Tyler Jacks (3 shared papers)Kristen C. Johnson (2 shared papers)Michael B. Yaffe (1 shared paper)Erik Wilker (1 shared paper)David Arthur Tuveson (1 shared paper)Marita J. Walmsley (1 shared paper)Anthony J. Capobianco (1 shared paper)
- Journals
- Molecular Cell (1 paper)Cancer Research (1 paper)Molecular and Cellular Biology (1 paper)Journal of Biological Chemistry (1 paper)
- Partner nations
- United StatesUnited Kingdom
In The Last Decade
Matthew S. Eckman
4 papers receiving 573 citations
Peers
Comparison fields: 5 of 52
- Cell Biology 240
- Neurology 208
- Cellular and Molecular Neuroscience 93
- Oncology 125
- Immunology and Allergy 28
Countries citing papers authored by Matthew S. Eckman
This map shows the geographic impact of Matthew S. Eckman'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 Matthew S. Eckman with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Matthew S. Eckman more than expected).
Fields of papers citing papers by Matthew S. Eckman
This network shows the impact of papers produced by Matthew S. Eckman. 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 Matthew S. Eckman. The network helps show where Matthew S. Eckman may publish in the future.
Co-authors
The 17 scholars most cited alongside Matthew S. Eckman, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.
All Works
| # | Work | ||
|---|---|---|---|
| 1 | 2003 | 207 | |
| 2 | 2002 | 205 | |
| 3 | 2007 | 142 | |
| 4 | 2005 | 34 |
About Matthew S. Eckman
Matthew S. Eckman is a scholar working on Cell Biology, Oncology, Molecular Biology, Neurology and Insect Science, having authored 4 papers that have together received 588 indexed citations. Recurring topics across this work include Wnt/β-catenin signaling in development and cancer (2 papers), Microtubule and mitosis dynamics (1 paper), Cellular Mechanics and Interactions (1 paper), PI3K/AKT/mTOR signaling in cancer (1 paper), Cancer-related Molecular Pathways (1 paper), Protein Kinase Regulation and GTPase Signaling (1 paper), Cell death mechanisms and regulation (1 paper) and Signaling Pathways in Disease (1 paper). The work is most often cited by research in Cell Biology (240 citations), Neurology (208 citations), Cellular and Molecular Neuroscience (93 citations), Oncology (125 citations) and Immunology and Allergy (28 citations). Matthew S. Eckman has collaborated with scholars based in United States and United Kingdom. Frequent co-authors include Joseph L. Kissil, Tyler Jacks, Kristen C. Johnson, Michael B. Yaffe, Erik Wilker, David Arthur Tuveson, Marita J. Walmsley, Anthony J. Capobianco, Carla F. Bender Kim and Haigis Kevin. Their work appears in journals such as Molecular Cell, Cancer Research, Molecular and Cellular Biology and Journal of Biological Chemistry.
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.