Hai Rao

11.1k total citations
54 papers, 1.9k citations indexed

About

Hai Rao is a scholar working on Molecular Biology, Cell Biology and Oncology. According to data from OpenAlex, Hai Rao has authored 54 papers receiving a total of 1.9k indexed citations (citations by other indexed papers that have themselves been cited), including 47 papers in Molecular Biology, 13 papers in Cell Biology and 11 papers in Oncology. Recurrent topics in Hai Rao's work include Ubiquitin and proteasome pathways (25 papers), Endoplasmic Reticulum Stress and Disease (9 papers) and Protein Degradation and Inhibitors (9 papers). Hai Rao is often cited by papers focused on Ubiquitin and proteasome pathways (25 papers), Endoplasmic Reticulum Stress and Disease (9 papers) and Protein Degradation and Inhibitors (9 papers). Hai Rao collaborates with scholars based in United States, China and Canada. Hai Rao's co-authors include Bruce Stillman, Ikjin Kim, Ashwani Sastry, York Marahrens, Kim Nasmyth, Frank Uhlmann, Alexander Varshavsky, Jennifer Apodaca, Kaixia Mi and Shiwen Luo and has published in prestigious journals such as Nature, Proceedings of the National Academy of Sciences and Journal of Biological Chemistry.

In The Last Decade

Hai Rao

51 papers receiving 1.9k citations

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
Hai Rao United States 23 1.7k 587 357 282 210 54 1.9k
Hideki Yashiroda Japan 24 1.9k 1.1× 843 1.4× 419 1.2× 462 1.6× 225 1.1× 31 2.2k
Svetlana Lyapina United States 9 1.9k 1.1× 445 0.8× 474 1.3× 286 1.0× 147 0.7× 13 2.1k
Julia K. Pagan United States 17 1.7k 1.0× 404 0.7× 510 1.4× 310 1.1× 152 0.7× 23 2.1k
Arno F. Alpi United Kingdom 24 1.8k 1.1× 333 0.6× 380 1.1× 204 0.7× 174 0.8× 35 2.1k
Hartmut Scheel Germany 16 1.6k 0.9× 436 0.7× 416 1.2× 219 0.8× 194 0.9× 19 1.9k
Robert Oania United States 9 1.7k 1.0× 619 1.1× 458 1.3× 462 1.6× 230 1.1× 9 1.8k
Claire Chu United States 5 1.7k 1.0× 416 0.7× 607 1.7× 217 0.8× 165 0.8× 10 1.9k
Adam G. Eldridge United States 13 1.1k 0.7× 359 0.6× 246 0.7× 126 0.4× 144 0.7× 15 1.4k
Philippe Coulombe France 23 2.2k 1.3× 367 0.6× 459 1.3× 106 0.4× 205 1.0× 30 2.5k
R. M. Renny Feldman United States 11 2.0k 1.1× 716 1.2× 533 1.5× 432 1.5× 150 0.7× 11 2.3k

Countries citing papers authored by Hai Rao

Since Specialization
Citations

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

Fields of papers citing papers by Hai Rao

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Hai Rao

This figure shows the co-authorship network connecting the top 25 collaborators of Hai Rao. A scholar is included among the top collaborators of Hai Rao 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 Hai Rao. Hai Rao 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.
Rao, Hai, et al.. (2025). Targeted degradation of α-synuclein by arginine-based PROTACs. Journal of Biological Chemistry. 301(8). 110449–110449. 3 indexed citations
2.
Chen, Xiao, Fengming Li, Xiaoxiao Song, et al.. (2025). Linker-free PROTACs efficiently induce the degradation of oncoproteins. Nature Communications. 16(1). 4794–4794. 10 indexed citations
4.
Mao, Chenyu, et al.. (2024). The ubiquitin ligase UBR4 and the deubiquitylase USP5 modulate the stability of DNA mismatch repair protein MLH1. Journal of Biological Chemistry. 300(8). 107592–107592.
5.
Yu, Yongjun, et al.. (2023). Single amino acid–based PROTACs trigger degradation of the oncogenic kinase BCR–ABL in chronic myeloid leukemia (CML). Journal of Biological Chemistry. 299(8). 104994–104994. 27 indexed citations
6.
Rao, Hai, et al.. (2022). How many authors does it take to publish a high profile or classic paper?. Molecular Biology of the Cell. 33(12). 3 indexed citations
7.
Yan, Zhengwei, Minzhang Cheng, Guohui Hu, et al.. (2021). Positive feedback of SuFu negating protein 1 on Hedgehog signaling promotes colorectal tumor growth. Cell Death and Disease. 12(2). 199–199. 14 indexed citations
9.
Shao, Jia, Linlin Xu, Limin Chen, et al.. (2017). Arl13b Promotes Gastric Tumorigenesis by Regulating Smo Trafficking and Activation of the Hedgehog Signaling Pathway. Cancer Research. 77(15). 4000–4013. 34 indexed citations
10.
Wang, Yao, Yong Li, Guanghui Hu, et al.. (2016). Nek2A phosphorylates and stabilizes SuFu: A new strategy of Gli2/Hedgehog signaling regulatory mechanism. Cellular Signalling. 28(9). 1304–1313. 13 indexed citations
11.
Bao, Xin, Jill L. Johnson, & Hai Rao. (2015). Rad25 Protein Is Targeted for Degradation by the Ubc4-Ufd4 Pathway. Journal of Biological Chemistry. 290(13). 8606–8612. 3 indexed citations
12.
Tang, Xiaoli, Libin Deng, Qi Chen, et al.. (2015). Inhibition of Hedgehog signaling pathway impedes cancer cell proliferation by promotion of autophagy. European Journal of Cell Biology. 94(5). 223–233. 18 indexed citations
13.
Chen, Qi, Rong Xu, Chunyan Zeng, et al.. (2014). Down-Regulation of Gli Transcription Factor Leads to the Inhibition of Migration and Invasion of Ovarian Cancer Cells via Integrin β4-Mediated FAK Signaling. PLoS ONE. 9(2). e88386–e88386. 69 indexed citations
14.
Krzeszinski, Jing Y., Vitnary Choe, Jia Shao, et al.. (2013). XPC promotes MDM2-mediated degradation of the p53 tumor suppressor. Molecular Biology of the Cell. 25(2). 213–221. 20 indexed citations
15.
Cheng, Haili, et al.. (2012). The Cdc48 Protein and Its Cofactor Vms1 Are Involved in Cdc13 Protein Degradation. Journal of Biological Chemistry. 287(32). 26788–26795. 13 indexed citations
16.
Kim, Ikjin, et al.. (2009). Usa1 Protein Facilitates Substrate Ubiquitylation through Two Separate Domains. PLoS ONE. 4(10). e7604–e7604. 12 indexed citations
17.
Kim, Ikjin, Kaixia Mi, & Hai Rao. (2004). Multiple Interactions of Rad23 Suggest a Mechanism for Ubiquitylated Substrate Delivery Important in Proteolysis. Molecular Biology of the Cell. 15(7). 3357–3365. 128 indexed citations
18.
Rao, Hai & Ashwani Sastry. (2002). Recognition of Specific Ubiquitin Conjugates Is Important for the Proteolytic Functions of the Ubiquitin-associated Domain Proteins Dsk2 and Rad23. Journal of Biological Chemistry. 277(14). 11691–11695. 171 indexed citations
19.
Bell, Stephen P., York Marahrens, Hai Rao, & Bruce Stillman. (1993). The Replicon Model and Eukaryotic Chromosomes. Cold Spring Harbor Symposia on Quantitative Biology. 58(0). 435–442. 8 indexed citations
20.
Rao, Hai, Scott C. Mohr, Heather Fairhead, & Peter Setlow. (1992). Synthesis and characterization of a 29‐amino acid residue DNA‐binding peptide derived from α/β‐type small, acid‐soluble spore proteins (SASP) of bacteria. FEBS Letters. 305(2). 115–120. 9 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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