John P. Alao

2.0k total citations · 1 hit paper
33 papers, 1.6k citations indexed

About

John P. Alao is a scholar working on Molecular Biology, Oncology and Organic Chemistry. According to data from OpenAlex, John P. Alao has authored 33 papers receiving a total of 1.6k indexed citations (citations by other indexed papers that have themselves been cited), including 26 papers in Molecular Biology, 7 papers in Oncology and 4 papers in Organic Chemistry. Recurrent topics in John P. Alao's work include DNA Repair Mechanisms (9 papers), Histone Deacetylase Inhibitors Research (9 papers) and Fungal and yeast genetics research (7 papers). John P. Alao is often cited by papers focused on DNA Repair Mechanisms (9 papers), Histone Deacetylase Inhibitors Research (9 papers) and Fungal and yeast genetics research (7 papers). John P. Alao collaborates with scholars based in Sweden, United Kingdom and Kenya. John P. Alao's co-authors include Per Sunnerhagen, R. Charles Coombes, David M. Vigushin, Eric W.‐F. Lam, Alexandra Stavropoulou, Peter Dinér, Simak Ali, Morten Grøtli, Máté Erdélyi and Abiy Yenesew and has published in prestigious journals such as Journal of Biological Chemistry, PLoS ONE and Cancer Research.

In The Last Decade

John P. Alao

32 papers receiving 1.6k citations

Hit Papers

The regulation of cyclin D1 degradation: roles in cancer ... 2007 2026 2013 2019 2007 200 400 600

Peers

John P. Alao
Numsen Hail United States
Darlene B. Royce United States
Baskaran Govindarajan United States
Hye‐Young Min South Korea
Numsen Hail United States
John P. Alao
Citations per year, relative to John P. Alao John P. Alao (= 1×) peers Numsen Hail

Countries citing papers authored by John P. Alao

Since Specialization
Citations

This map shows the geographic impact of John P. Alao'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 John P. Alao with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites John P. Alao more than expected).

Fields of papers citing papers by John P. Alao

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by John P. Alao. 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 John P. Alao. The network helps show where John P. Alao may publish in the future.

Co-authorship network of co-authors of John P. Alao

This figure shows the co-authorship network connecting the top 25 collaborators of John P. Alao. A scholar is included among the top collaborators of John P. Alao based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with John P. Alao. John P. Alao is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

20 of 20 papers shown
1.
Alao, John P., Juhi Kumar, Despina Stamataki, & Charalampos Rallis. (2025). Dissecting the cell cycle regulation, DNA damage sensitivity and lifespan effects of caffeine in fission yeast. Microbial Cell. 12. 141–156.
2.
Alao, John P., et al.. (2023). Interplays of AMPK and TOR in Autophagy Regulation in Yeast. Cells. 12(4). 519–519. 17 indexed citations
3.
Alao, John P., et al.. (2015). Suppression of Sensitivity to Drugs and Antibiotics by High External Cation Concentrations in Fission Yeast. PLoS ONE. 10(3). e0119297–e0119297. 4 indexed citations
4.
Alao, John P., et al.. (2014). Selective inhibition of RET mediated cell proliferation in vitro by the kinase inhibitor SPP86. BMC Cancer. 14(1). 853–853. 16 indexed citations
5.
Poon, Jia‐Fei, John P. Alao, Per Sunnerhagen, & Peter Dinér. (2013). Azastilbenes: a cut-off to p38 MAPK inhibitors. Organic & Biomolecular Chemistry. 11(27). 4526–4526. 5 indexed citations
6.
Endale, Milkyas, John P. Alao, Hoseah M. Akala, et al.. (2011). Antiplasmodial Quinones fromPentas longifloraandPentas lanceolata. Planta Medica. 78(1). 31–35. 22 indexed citations
8.
Alao, John P., et al.. (2009). Inhibition of type I histone deacetylase increases resistance of checkpoint-deficient cells to genotoxic agents through mitotic delay. Molecular Cancer Therapeutics. 8(9). 2606–2615. 5 indexed citations
9.
Alao, John P. & Per Sunnerhagen. (2009). The ATM and ATR inhibitors CGK733 and caffeine suppress cyclin D1 levels and inhibit cell proliferation. Radiation Oncology. 4(1). 51–51. 41 indexed citations
10.
Alao, John P. & Per Sunnerhagen. (2008). Rad3 and Sty1 function in Schizosaccharomyces pombe: an integrated response to DNA damage and environmental stress?. Molecular Microbiology. 68(2). 246–254. 14 indexed citations
11.
Alao, John P.. (2007). The regulation of cyclin D1 degradation: roles in cancer development and the potential for therapeutic invention. Molecular Cancer. 6(1). 24–24. 698 indexed citations breakdown →
12.
Marson, Charles M., Stéphane Sengmany, John P. Alao, et al.. (2006). Structure–activity relationships of aryloxyalkanoic acid hydroxyamides as potent inhibitors of histone deacetylase. Bioorganic & Medicinal Chemistry Letters. 17(1). 136–141. 16 indexed citations
13.
Alao, John P., Simon C. Gamble, Alexandra Stavropoulou, et al.. (2006). The cyclin D1 proto-oncogene is sequestered in the cytoplasm of mammalian cancer cell lines. Molecular Cancer. 5(1). 7–7. 63 indexed citations
14.
Alao, John P., Alexandra Stavropoulou, Eric W.‐F. Lam, & R. Charles Coombes. (2006). Role of glycogen synthase kinase 3 beta (GSK3beta) in mediating the cytotoxic effects of the histone deacetylase inhibitor trichostatin A (TSA) in MCF-7 breast cancer cells.. Molecular Cancer. 5(1). 40–40. 39 indexed citations
15.
Alao, John P., Alexandra Stavropoulou, Eric W.‐F. Lam, R. Charles Coombes, & David M. Vigushin. (2006). Histone deacetylase inhibitor, Trichostatin A induces ubiquitin-dependent cyclin D1 degradation in MCF-7 breast cancer cells. Molecular Cancer. 5(1). 8–8. 73 indexed citations
16.
Leyton, Julius, John P. Alao, Marco Da Costa, et al.. (2006). In vivoBiological Activity of the Histone Deacetylase Inhibitor LAQ824 Is detectable with 3′-Deoxy-3′-[18F]Fluorothymidine Positron Emission Tomography. Cancer Research. 66(15). 7621–7629. 59 indexed citations
17.
Sanderson, Lisa, Graham W. Taylor, Eric O. Aboagye, et al.. (2004). PLASMA PHARMACOKINETICS AND METABOLISM OF THE HISTONE DEACETYLASE INHIBITOR TRICHOSTATIN A AFTER INTRAPERITONEAL ADMINISTRATION TO MICE. Drug Metabolism and Disposition. 32(10). 1132–1138. 74 indexed citations
18.
Varshochi, Rana, Andrew Sunters, John P. Alao, et al.. (2004). ICI182,780 Induces p21 Gene Transcription through Releasing Histone Deacetylase 1 and Estrogen Receptor α from Sp1 Sites to Induce Cell Cycle Arrest in MCF-7 Breast Cancer Cell Line. Journal of Biological Chemistry. 280(5). 3185–3196. 59 indexed citations
19.
Marson, Charles M., et al.. (2004). Stereodefined and polyunsaturated inhibitors of histone deacetylase based on (2E,4E)-5-arylpenta-2,4-dienoic acid hydroxyamides. Bioorganic & Medicinal Chemistry Letters. 14(10). 2477–2481. 16 indexed citations
20.
Vigushin, David M., Yuan-Lin Dong, Lindsey Inman, et al.. (2004). The Nuclear Oxysterol Receptor LXRα Is Expressed in the Normal Human Breast and in Breast Cancer. Medical Oncology. 21(2). 123–132. 28 indexed citations

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.

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