Mark T. Keating
Impact in
- Cardiology and Cardiovascular Medicine top 0.01%
- Cardiac electrophysiology and arrhythmias
- Cardiomyopathy and Myosin Studies
- Cardiac pacing and defibrillation studies
- Developmental Neuroscience top 0.1%
- Williams Syndrome Research
Papers in
-
- Ion channel regulation and function 32
- Congenital heart defects research 10
- Developmental Biology and Gene Regulation 9
- Receptor Mechanisms and Signaling 6
-
- Cardiac electrophysiology and arrhythmias 49
- Cardiomyopathy and Myosin Studies 12
- Co-authors
- Michael C. Sanguinetti (19 shared papers)Mark Curran (13 shared papers)Igor Splawski (21 shared papers)Katherine W. Timothy (19 shared papers)Kenneth D. Poss (7 shared papers)Donald L. Atkinson (9 shared papers)Peter J. Schwartz (14 shared papers)Jeffrey A. Towbin (10 shared papers)
- Journals
- Circulation (10 papers)Journal of Biological Chemistry (9 papers)Cell (8 papers)Science (6 papers)Proceedings of the National Academy of Sciences (6 papers)
- Partner nations
- United StatesItalyPoland
In The Last Decade
Mark T. Keating
117 papers receiving 31.0k citations
Mark T. Keating's Hit Papers
Peers
Comparison fields: 5 of 161
- Cardiology and Cardiovascular Medicine 19.1k
- Developmental Neuroscience 1.7k
- Molecular Biology 20.9k
- Cellular and Molecular Neuroscience 4.5k
- Cell Biology 1.8k
Countries citing papers authored by Mark T. Keating
This map shows the geographic impact of Mark T. Keating'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 Mark T. Keating with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Mark T. Keating more than expected).
Fields of papers citing papers by Mark T. Keating
This network shows the impact of papers produced by Mark T. Keating. 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 Mark T. Keating. The network helps show where Mark T. Keating may publish in the future.
Co-authors
The 25 scholars most cited alongside Mark T. Keating, 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 117 papers — load more, or switch the sort, to bring in the rest.
| # | Work | ||
|---|---|---|---|
| 1 | A mechanistic link between an inherited and an acquird cardiac arrthytmia: HERG encodes the IKr potassium channel Hit paper breakdown → | 1995 | 2000 |
| 2 | A molecular basis for cardiac arrhythmia: HERG mutations cause long QT syndrome Hit paper breakdown → | 1995 | 1750 |
| 3 | Heart Regeneration in Zebrafish Hit paper breakdown → | 2002 | 1441 |
| 4 | Coassembly of KVLQT1 and minK (IsK) proteins to form cardiac IKS potassium channel Hit paper breakdown → | 1996 | 1432 |
| 5 | Positional cloning of a novel potassium channel gene: KVLQT1 mutations cause cardiac arrhythmias Hit paper breakdown → | 1996 | 1329 |
| 6 | Genetic basis and molecular mechanism for idiopathic ventricular fibrillation Hit paper breakdown → | 1998 | 1260 |
| 7 | SCN5A mutations associated with an inherited cardiac arrhythmia, long QT syndrome Hit paper breakdown → | 1995 | 1256 |
| 8 | CaV1.2 Calcium Channel Dysfunction Causes a Multisystem Disorder Including Arrhythmia and Autism Hit paper breakdown → | 2004 | 1124 |
| 9 | MiRP1 Forms IKr Potassium Channels with HERG and Is Associated with Cardiac Arrhythmia Hit paper breakdown → | 1999 | 1008 |
| 10 | Spectrum of Mutations in Long-QT Syndrome Genes Hit paper breakdown → | 2000 | 958 |
| 11 | Hemizygosity at the elastin locus in a developmental disorder, Williams syndrome Hit paper breakdown → | 1993 | 813 |
| 12 | Molecular and Cellular Mechanisms of Cardiac Arrhythmias Hit paper breakdown → | 2001 | 764 |
| 13 | Long QT Syndrome Patients With Mutations of the SCN5A and HERG Genes Have Differential Responses to Na + Channel Blockade and to Increases in Heart Rate Hit paper breakdown → | 1995 | 584 |
| 14 | Mutations in the hminK gene cause long QT syndrome and suppress lKs function Hit paper breakdown → | 1997 | 581 |
| 15 | Elastin is an essential determinant of arterial morphogenesis Hit paper breakdown → | 1998 | 581 |
| 16 | Influence of the Genotype on the Clinical Course of the Long-QT Syndrome Hit paper breakdown → | 1998 | 505 |
| 17 | Periostin induces proliferation of differentiated cardiomyocytes and promotes cardiac repair Hit paper breakdown → | 2007 | 502 |
| 18 | 1998 | 481 | |
| 19 | 2005 | 461 | |
| 20 | 2005 | 453 |
About Mark T. Keating
Mark T. Keating is a scholar working on Molecular Biology, Cardiology and Cardiovascular Medicine, Cell Biology, Developmental Neuroscience and Surgery, having authored 117 papers that have together received 31.8k indexed citations. Recurring topics across this work include Cardiac electrophysiology and arrhythmias (49 papers), Ion channel regulation and function (32 papers), Williams Syndrome Research (13 papers), Cardiomyopathy and Myosin Studies (12 papers), Congenital heart defects research (10 papers), Developmental Biology and Gene Regulation (9 papers), Receptor Mechanisms and Signaling (6 papers) and Hippo pathway signaling and YAP/TAZ (6 papers). The work is most often cited by research in Cardiology and Cardiovascular Medicine (19.1k citations), Developmental Neuroscience (1.7k citations), Molecular Biology (20.9k citations), Cellular and Molecular Neuroscience (4.5k citations) and Cell Biology (1.8k citations). Mark T. Keating has collaborated with scholars based in United States, Italy and Poland. Frequent co-authors include Michael C. Sanguinetti, Mark Curran, Igor Splawski, Katherine W. Timothy, Kenneth D. Poss, Donald L. Atkinson, Peter J. Schwartz, Jeffrey A. Towbin, Jiaxiang Shen and Michael H. Lehmann. Their work appears in journals such as Circulation, Journal of Biological Chemistry, Cell, Science and Proceedings of the National Academy of Sciences.
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.