Ann Seman
Impact in
-
- Immune Cell Function and Interaction
- T-cell and B-cell Immunology
- Immunodeficiency and Autoimmune Disorders
-
- Whipple's Disease and Interleukins
Papers in
-
- Mitochondrial Function and Pathology 2
- Congenital heart defects research 1
-
- Whipple's Disease and Interleukins 2
- Co-authors
- William W. Cruikshank (2 shared papers)William Brazer (2 shared papers)Thomas C. Ryan (2 shared papers)P. Hemachandra Reddy (1 shared paper)Jangampalli Adi Pradeepkiran (1 shared paper)David M. Center (1 shared paper)Joan M. Stoler (2 shared papers)Qihua Fu (1 shared paper)
- Journals
- BMC Genomics (1 paper)The Journal of Immunology (1 paper)The Neuroscientist (1 paper)American Journal of Medical Genetics Part A (1 paper)PubMed (1 paper)
- Partner nations
- United StatesOmanChina
In The Last Decade
Ann Seman
5 papers receiving 209 citations
Peers
Comparison fields: 5 of 52
- Immunology 61
- Pathology and Forensic Medicine 42
- Immunology and Allergy 12
- Genetics 41
- Sensory Systems 7
Countries citing papers authored by Ann Seman
This map shows the geographic impact of Ann Seman'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 Ann Seman with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Ann Seman more than expected).
Fields of papers citing papers by Ann Seman
This network shows the impact of papers produced by Ann Seman. 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 Ann Seman. The network helps show where Ann Seman may publish in the future.
Co-authors
The 25 scholars most cited alongside Ann Seman, 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 | 2014 | 60 | |
| 2 | Reciprocal desensitization of CCR5 and CD4 is mediated by IL-16 and macrophage-inflammatory protein-1 beta, respectively. | 1999 | 44 |
| 3 | 1999 | 41 | |
| 4 | 2015 | 37 | |
| 5 | 2023 | 33 |
About Ann Seman
Ann Seman is a scholar working on Molecular Biology, Pathology and Forensic Medicine, Genetics, Immunology and Virology, having authored 5 papers that have together received 215 indexed citations. Recurring topics across this work include Mitochondrial Function and Pathology (2 papers), Immune Cell Function and Interaction (2 papers), Whipple's Disease and Interleukins (2 papers), Congenital heart defects research (1 paper), HIV Research and Treatment (1 paper), Autophagy in Disease and Therapy (1 paper), Alzheimer's disease research and treatments (1 paper) and Genomics and Rare Diseases (1 paper). The work is most often cited by research in Immunology (61 citations), Pathology and Forensic Medicine (42 citations), Immunology and Allergy (12 citations), Genetics (41 citations) and Sensory Systems (7 citations). Ann Seman has collaborated with scholars based in United States, Oman and China. Frequent co-authors include William W. Cruikshank, William Brazer, Thomas C. Ryan, P. Hemachandra Reddy, Jangampalli Adi Pradeepkiran, David M. Center, Joan M. Stoler, Qihua Fu, Zhaojing Zheng and Jian Wang. Their work appears in journals such as BMC Genomics, The Journal of Immunology, The Neuroscientist, American Journal of Medical Genetics Part A and PubMed.
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.