Aleksandra Dakic

2.1k total citations · 1 hit paper
17 papers, 1.1k citations indexed

About

Aleksandra Dakic is a scholar working on Molecular Biology, Physiology and Epidemiology. According to data from OpenAlex, Aleksandra Dakic has authored 17 papers receiving a total of 1.1k indexed citations (citations by other indexed papers that have themselves been cited), including 12 papers in Molecular Biology, 9 papers in Physiology and 6 papers in Epidemiology. Recurrent topics in Aleksandra Dakic's work include Telomeres, Telomerase, and Senescence (9 papers), Cervical Cancer and HPV Research (5 papers) and Molecular Biology Techniques and Applications (4 papers). Aleksandra Dakic is often cited by papers focused on Telomeres, Telomerase, and Senescence (9 papers), Cervical Cancer and HPV Research (5 papers) and Molecular Biology Techniques and Applications (4 papers). Aleksandra Dakic collaborates with scholars based in United States, China and Germany. Aleksandra Dakic's co-authors include Xuefeng Liu, Richard Schlegel, Vera Simić, Yiyu Zhang, Bhaskar Kallakury, Bassem R. Haddad, Olga Timofeeva, Chris Albanese, Renxiang Chen and Anatoly Dritschilo and has published in prestigious journals such as Proceedings of the National Academy of Sciences, Cancer Research and Journal of Virology.

In The Last Decade

Aleksandra Dakic

17 papers receiving 1.1k citations

Hit Papers

ROCK Inhibitor and Feeder Cells Induce the Conditional Re... 2011 2026 2016 2021 2011 100 200 300 400 500

Peers

Aleksandra Dakic
Sandra Chapman United States
Bart Jonckx Belgium
Brian Cao United States
Stephen Fitter Australia
Carl J. DeSelm United States
Frank Traub Germany
S Saga Japan
Kwun Wah Wen United States
Sandra Chapman United States
Aleksandra Dakic
Citations per year, relative to Aleksandra Dakic Aleksandra Dakic (= 1×) peers Sandra Chapman

Countries citing papers authored by Aleksandra Dakic

Since Specialization
Citations

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

Fields of papers citing papers by Aleksandra Dakic

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Aleksandra Dakic. 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 Aleksandra Dakic. The network helps show where Aleksandra Dakic may publish in the future.

Co-authorship network of co-authors of Aleksandra Dakic

This figure shows the co-authorship network connecting the top 25 collaborators of Aleksandra Dakic. A scholar is included among the top collaborators of Aleksandra Dakic 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 Aleksandra Dakic. Aleksandra Dakic is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

17 of 17 papers shown
1.
Gong, Weiyi, Aleksandra Dakic, Nagireddy Putluri, et al.. (2025). Canonical and non-canonical functions of the non-coding RNA component (TERC) of telomerase complex. Cell & Bioscience. 15(1). 30–30. 1 indexed citations
2.
Dakic, Aleksandra, Qi‐En Wang, Darrion Mitchell, et al.. (2024). Noncanonical functions of telomerase and telomeres in viruses‐associated cancer. Journal of Medical Virology. 96(5). e29665–e29665. 7 indexed citations
3.
Dakic, Aleksandra, Megan E. Spurgeon, Bhaskar Kallakury, et al.. (2022). AIB1 is a novel target of the high‐risk HPV E6 protein and a biomarker of cervical cancer progression. Journal of Medical Virology. 94(8). 3962–3977. 7 indexed citations
4.
Mondal, Abdul M., Hua Zhou, Izumi Horikawa, et al.. (2018). Δ133p53α, a natural p53 isoform, contributes to conditional reprogramming and long-term proliferation of primary epithelial cells. Cell Death and Disease. 9(7). 750–750. 25 indexed citations
5.
Zhou, Hua, et al.. (2018). Time-Dependent Effects of POT1 Knockdown on Proliferation, Tumorigenicity, and HDACi Response of SK-OV3 Ovarian Cancer Cells. BioMed Research International. 2018. 1–12. 5 indexed citations
6.
Zhang, Yiyu, Aleksandra Dakic, Renxiang Chen, et al.. (2017). Direct HPV E6/Myc interactions induce histone modifications, Pol II phosphorylation, and hTERT promoter activation. Oncotarget. 8(56). 96323–96339. 37 indexed citations
7.
Liu, Xuefeng, Ewa Krawczyk, Nancy Palechor-Ceron, et al.. (2016). Abstract 4256: Functional analysis for cancer precision medicine using patient-derived 2D and 3D cell models. Cancer Research. 76(14_Supplement). 4256–4256. 2 indexed citations
8.
Dakic, Aleksandra, Kyle A. DiVito, Frank A. Suprynowicz, et al.. (2016). ROCK inhibitor reduces Myc-induced apoptosis and mediates immortalization of human keratinocytes. Oncotarget. 7(41). 66740–66753. 33 indexed citations
9.
Selvanathan, Saravana P., Garrett T. Graham, Hayriye V. Erkizan, et al.. (2015). Oncogenic fusion protein EWS-FLI1 is a network hub that regulates alternative splicing. Proceedings of the National Academy of Sciences. 112(11). E1307–16. 105 indexed citations
10.
Liu, Xuefeng, Ewa Krawczyk, Nancy Palechor-Ceron, et al.. (2014). Abstract 2972: Conditionally reprogrammed cells (CRCs): A new model for cancer research and personalized medicine. Cancer Research. 74(19_Supplement). 2972–2972. 1 indexed citations
11.
Palechor-Ceron, Nancy, Frank A. Suprynowicz, Geeta Upadhyay, et al.. (2013). Radiation Induces Diffusible Feeder Cell Factor(s) That Cooperate with ROCK Inhibitor to Conditionally Reprogram and Immortalize Epithelial Cells. American Journal Of Pathology. 183(6). 1862–1870. 88 indexed citations
12.
Dakic, Aleksandra, Renxiang Chen, Nancy Palechor-Ceron, et al.. (2013). HPV16 E7 Protein and hTERT Proteins Defective for Telomere Maintenance Cooperate to Immortalize Human Keratinocytes. PLoS Pathogens. 9(4). e1003284–e1003284. 36 indexed citations
13.
Liu, Xuefeng, Virginie Ory, Sandra Chapman, et al.. (2011). ROCK Inhibitor and Feeder Cells Induce the Conditional Reprogramming of Epithelial Cells. American Journal Of Pathology. 180(2). 599–607. 554 indexed citations breakdown →
14.
Liu, Xuefeng, Aleksandra Dakic, Yiyu Zhang, et al.. (2009). HPV E6 protein interacts physically and functionally with the cellular telomerase complex. Proceedings of the National Academy of Sciences. 106(44). 18780–18785. 100 indexed citations
15.
Liu, Xuefeng, Jeffrey Roberts, Aleksandra Dakic, Yiyu Zhang, & Richard Schlegel. (2008). HPV E7 contributes to the telomerase activity of immortalized and tumorigenic cells and augments E6-induced hTERT promoter function. Virology. 375(2). 611–623. 71 indexed citations
16.
Liu, Xuefeng, Aleksandra Dakic, Renxiang Chen, et al.. (2008). Cell-Restricted Immortalization by Human Papillomavirus Correlates with Telomerase Activation and Engagement of the hTERT Promoter by Myc. Journal of Virology. 82(23). 11568–11576. 56 indexed citations
17.
Nićiforović, Ana, et al.. (2004). Flow cytometry evaluation of HeLa S3 cell death induced by gamma-radiation. Digital Object Identifier (DOI) Repository Serbia (National Library of Serbia). 23(2). 135–142. 3 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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