Prem Khanal

872 total citations
20 papers, 721 citations indexed

About

Prem Khanal is a scholar working on Molecular Biology, Cell Biology and Oncology. According to data from OpenAlex, Prem Khanal has authored 20 papers receiving a total of 721 indexed citations (citations by other indexed papers that have themselves been cited), including 17 papers in Molecular Biology, 8 papers in Cell Biology and 4 papers in Oncology. Recurrent topics in Prem Khanal's work include Signaling Pathways in Disease (7 papers), Hippo pathway signaling and YAP/TAZ (7 papers) and PI3K/AKT/mTOR signaling in cancer (3 papers). Prem Khanal is often cited by papers focused on Signaling Pathways in Disease (7 papers), Hippo pathway signaling and YAP/TAZ (7 papers) and PI3K/AKT/mTOR signaling in cancer (3 papers). Prem Khanal collaborates with scholars based in Canada, South Korea and United States. Prem Khanal's co-authors include Xiaolong Yang, Taha Azad, Hong Seok Choi, Helena J. Janse van Rensburg, Yawei Hao, Michael J. Rauh, Ling Min, Brooke Snetsinger, Charles H. Graham and Lori M. Minassian and has published in prestigious journals such as Journal of Biological Chemistry, Cancer Research and Oncogene.

In The Last Decade

Prem Khanal

20 papers receiving 718 citations

Peers — A (Enhanced Table)

Peers by citation overlap · career bar shows stage (early→late) cites · hero ref

Name h Career Trend Papers Cites
Prem Khanal Canada 14 460 322 241 133 63 20 721
Rosanna Dattilo Italy 11 449 1.0× 322 1.0× 295 1.2× 64 0.5× 133 2.1× 13 800
Alessandro Zannini Italy 9 467 1.0× 209 0.6× 273 1.1× 99 0.7× 156 2.5× 10 773
Anita Hufnagel Germany 13 456 1.0× 124 0.4× 160 0.7× 130 1.0× 86 1.4× 15 633
Ron Bumeister United States 9 512 1.1× 105 0.3× 114 0.5× 155 1.2× 86 1.4× 10 683
Daniel Grun United States 14 394 0.9× 158 0.5× 197 0.8× 64 0.5× 75 1.2× 17 637
Staci N. Keller United States 10 742 1.6× 290 0.9× 91 0.4× 102 0.8× 56 0.9× 15 844
Nancy E. Dreckschmidt United States 11 532 1.2× 87 0.3× 189 0.8× 74 0.6× 104 1.7× 16 793
Rosa Della Monica Italy 12 406 0.9× 127 0.4× 177 0.7× 34 0.3× 83 1.3× 32 610
Jeremy A. Hengst United States 16 456 1.0× 205 0.6× 65 0.3× 82 0.6× 54 0.9× 30 576
Jingjing Ma China 12 281 0.6× 178 0.6× 99 0.4× 123 0.9× 112 1.8× 33 589

Countries citing papers authored by Prem Khanal

Since Specialization
Citations

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

Fields of papers citing papers by Prem Khanal

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Prem Khanal

This figure shows the co-authorship network connecting the top 25 collaborators of Prem Khanal. A scholar is included among the top collaborators of Prem Khanal 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 Prem Khanal. Prem Khanal 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.
Khanal, Prem, et al.. (2023). Characterization of a phenotypically severe animal model for human AB-Variant GM2 gangliosidosis. Frontiers in Molecular Neuroscience. 16. 1242814–1242814. 2 indexed citations
2.
Khanal, Prem, Melissa Mitchell, Zhilin Chen, et al.. (2023). Biochemical Correction of GM2 Ganglioside Accumulation in AB-Variant GM2 Gangliosidosis. International Journal of Molecular Sciences. 24(11). 9217–9217. 4 indexed citations
3.
Zhao, Yulei, Calvin Sjaarda, Prem Khanal, et al.. (2019). A one-step tRNA-CRISPR system for genome-wide genetic interaction mapping in mammalian cells. Scientific Reports. 9(1). 14499–14499. 6 indexed citations
4.
Khanal, Prem, Benjamin Yeung, Yulei Zhao, & Xiaolong Yang. (2019). Identification of Prolyl isomerase Pin1 as a novel positive regulator of YAP/TAZ in breast cancer cells. Scientific Reports. 9(1). 6394–6394. 18 indexed citations
5.
Azad, Taha, Kazem Nouri, Helena J. Janse van Rensburg, et al.. (2019). A gain-of-functional screen identifies the Hippo pathway as a central mediator of receptor tyrosine kinases during tumorigenesis. Oncogene. 39(2). 334–355. 51 indexed citations
6.
Nouri, Kazem, Taha Azad, Elizabeth D. Lightbody, et al.. (2019). A kinome‐wide screen using a NanoLuc LATS luminescent biosensor identifies ALK as a novel regulator of the Hippo pathway in tumorigenesis and immune evasion. The FASEB Journal. 33(11). 12487–12499. 34 indexed citations
7.
Rensburg, Helena J. Janse van, Taha Azad, Ling Min, et al.. (2018). The Hippo Pathway Component TAZ Promotes Immune Evasion in Human Cancer through PD-L1. Cancer Research. 78(6). 1457–1470. 244 indexed citations
8.
Yeung, Benjamin, et al.. (2018). Identification of Cdk1–LATS–Pin1 as a Novel Signaling Axis in Anti-tubulin Drug Response of Cancer Cells. Molecular Cancer Research. 16(6). 1035–1045. 19 indexed citations
9.
Khanal, Prem, Zongchao Jia, & Xiaolong Yang. (2018). Cysteine residues are essential for dimerization of Hippo pathway components YAP2L and TAZ. Scientific Reports. 8(1). 3485–3485. 12 indexed citations
10.
Zhao, Yulei, Prem Khanal, Paul B. Savage, et al.. (2014). YAP-Induced Resistance of Cancer Cells to Antitubulin Drugs Is Modulated by a Hippo-Independent Pathway. Cancer Research. 74(16). 4493–4503. 80 indexed citations
11.
Yun, Hyo Jeong, Garam Kım, Prem Khanal, et al.. (2013). Inhibitory Effects of a New 1<i>H</i>-Pyrrolo[3,2-<i>c</i>]pyridine Derivative, KIST101029, on Activator Protein-1 Activity and Neoplastic Cell Transformation Induced by Insulin-Like Growth Factor-1. Biological and Pharmaceutical Bulletin. 36(9). 1466–1473. 2 indexed citations
12.
Khanal, Prem, et al.. (2013). Prolyl isomerase Pin1 negatively regulates the stability of SUV39H1 to promote tumorigenesis in breast cancer. The FASEB Journal. 27(11). 4606–4618. 32 indexed citations
13.
Kım, Garam, Prem Khanal, Jin Young Kim, et al.. (2013). COT phosphorylates prolyl-isomerase Pin1 to promote tumorigenesis in breast cancer. Molecular Carcinogenesis. 54(6). 440–448. 30 indexed citations
14.
Khanal, Prem, et al.. (2012). The prolyl isomerase Pin1 interacts with and downregulates the activity of AMPK leading to induction of tumorigenicity of hepatocarcinoma cells. Molecular Carcinogenesis. 52(10). 813–823. 14 indexed citations
15.
16.
Khanal, Prem, Sung‐Chul Lim, Sang‐Gun Ahn, et al.. (2011). Proyl isomerase Pin1 facilitates ubiquitin-mediated degradation of cyclin-dependent kinase 10 to induce tamoxifen resistance in breast cancer cells. Oncogene. 31(34). 3845–3856. 42 indexed citations
17.
Khanal, Prem, et al.. (2011). Aglycon of Rhizochalin from the Rhizochalina incrustata Induces Apoptosis via Activation of AMP-Activated Protein Kinase in HT-29 Colon Cancer Cells. Biological and Pharmaceutical Bulletin. 34(10). 1553–1558. 21 indexed citations
18.
19.
Khanal, Prem, et al.. (2010). The Prolyl Isomerase Pin1 Induces LC-3 Expression and Mediates Tamoxifen Resistance in Breast Cancer. Journal of Biological Chemistry. 285(31). 23829–23841. 47 indexed citations
20.

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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