Bulavin Dv
Impact in
- Oncology top 10%
- Cancer-related Molecular Pathways
-
- Cell death mechanisms and regulation
- DNA Repair Mechanisms
- Melanoma and MAPK Pathways
- Ubiquitin and proteasome pathways
- Epigenetics and DNA Methylation
- RNA modifications and cancer
Papers in
- Oncology 5
- Cancer-related Molecular Pathways 5
-
- Cell death mechanisms and regulation 2
- Glutathione Transferases and Polymorphisms 1
- Co-authors
- Smirnov Vv (1 shared paper)
- Journals
- The EMBO Journal (1 paper)PubMed (5 papers)
- Partner nations
- RussiaUnited StatesJapan
In The Last Decade
Bulavin Dv
5 papers receiving 581 citations
Bulavin Dv's Hit Papers
Peers
Comparison fields: 5 of 69
- Oncology 277
- Molecular Biology 456
- Cancer Research 89
- Biotechnology 48
- Aging 8
Countries citing papers authored by Bulavin Dv
This map shows the geographic impact of Bulavin Dv'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 Bulavin Dv with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Bulavin Dv more than expected).
Fields of papers citing papers by Bulavin Dv
This network shows the impact of papers produced by Bulavin Dv. 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 Bulavin Dv. The network helps show where Bulavin Dv may publish in the future.
Co-authors
The 1 scholars most cited alongside Bulavin Dv, 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 | Phosphorylation of human p53 by p38 kinase coordinates N‐terminal phosphorylation and apoptosis in response to UV radiation Hit paper breakdown → | 1999 | 583 |
| 2 | [The subcellular distribution of the glutathione system enzymes in the brain tissue of the rat]. | 1993 | 2 |
| 3 | [Oncoproteins E1Aad5 interact with universal inhibitor of cyclin-dependent kinases p21/waf-1 and inhibit its activity in E1A + cHa-ras transformants]. | 2000 | 2 |
| 4 | [Anti-apoptotic and antiproliferative effect of bcl-2 gene transferred to E1A+cHa-ras-transformed cells]. | 2002 | 1 |
| 5 | [Function of the p53-pRb-dependent path after exposure to DNA damaging agents in rats embryonal fibroblast cells, transformed by E1A and Ha-Ras oncogenes]. | 1998 | 1 |
| 6 | [Apoptotic cell death in rat embryo fibroblasts transformed by EiA + cHa-RAS oncogenes after gamma irradiation]. | 1998 | 0 |
About Bulavin Dv
Bulavin Dv is a scholar working on Oncology, Molecular Biology, Biotechnology, Cancer Research and Infectious Diseases, having authored 6 papers that have together received 589 indexed citations. Recurring topics across this work include Cancer-related Molecular Pathways (5 papers), Cell death mechanisms and regulation (2 papers), Glutathione Transferases and Polymorphisms (1 paper), Cancer, Hypoxia, and Metabolism (1 paper) and Cancer Research and Treatments (1 paper). The work is most often cited by research in Oncology (277 citations), Molecular Biology (456 citations), Cancer Research (89 citations), Biotechnology (48 citations) and Aging (8 citations). Bulavin Dv has collaborated with scholars based in Russia, United States and Japan. Frequent co-authors include Smirnov Vv. Their work appears in journals such as The EMBO Journal 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.