William Paradee

1.2k total citations
20 papers, 915 citations indexed

About

William Paradee is a scholar working on Genetics, Molecular Biology and Cognitive Neuroscience. According to data from OpenAlex, William Paradee has authored 20 papers receiving a total of 915 indexed citations (citations by other indexed papers that have themselves been cited), including 12 papers in Genetics, 11 papers in Molecular Biology and 3 papers in Cognitive Neuroscience. Recurrent topics in William Paradee's work include Genetics and Neurodevelopmental Disorders (12 papers), Epigenetics and DNA Methylation (5 papers) and Genomic variations and chromosomal abnormalities (4 papers). William Paradee is often cited by papers focused on Genetics and Neurodevelopmental Disorders (12 papers), Epigenetics and DNA Methylation (5 papers) and Genomic variations and chromosomal abnormalities (4 papers). William Paradee collaborates with scholars based in United States, China and Poland. William Paradee's co-authors include Jeremy C. Smith, Thomas W. Glover, Charles M. Wilke, Stephen T. Warren, P. Jeffrey Conn, Haley E. Melikian, Aileen Kenneson, Bryan K. Hall, Chadwick Mullins and Ravi Shridhar and has published in prestigious journals such as Proceedings of the National Academy of Sciences, Journal of Biological Chemistry and The Journal of Experimental Medicine.

In The Last Decade

William Paradee

19 papers receiving 898 citations

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
William Paradee United States 12 598 586 197 111 91 20 915
Daniela Orteschi Italy 19 597 1.0× 467 0.8× 155 0.8× 55 0.5× 71 0.8× 37 917
Alexei Stortchevoi United States 12 335 0.6× 828 1.4× 115 0.6× 159 1.4× 66 0.7× 18 988
Marijke Bauters Belgium 17 911 1.5× 809 1.4× 199 1.0× 54 0.5× 45 0.5× 25 1.3k
Nandita Quaderi Italy 12 387 0.6× 655 1.1× 88 0.4× 35 0.3× 126 1.4× 18 849
Lachlan A. Jolly Australia 18 465 0.8× 881 1.5× 51 0.3× 154 1.4× 64 0.7× 29 1.2k
Donna M. Muzny United States 15 456 0.8× 551 0.9× 103 0.5× 23 0.2× 54 0.6× 20 854
Gotthold Barbi Germany 17 632 1.1× 560 1.0× 130 0.7× 52 0.5× 22 0.2× 59 1.1k
Jiong Yan United States 15 487 0.8× 650 1.1× 33 0.2× 73 0.7× 92 1.0× 27 1.0k
David C. Ward United States 15 267 0.4× 805 1.4× 51 0.3× 93 0.8× 90 1.0× 19 1.3k
Matthew Pastore United States 12 450 0.8× 605 1.0× 291 1.5× 24 0.2× 44 0.5× 23 940

Countries citing papers authored by William Paradee

Since Specialization
Citations

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

Fields of papers citing papers by William Paradee

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of William Paradee

This figure shows the co-authorship network connecting the top 25 collaborators of William Paradee. A scholar is included among the top collaborators of William Paradee 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 William Paradee. William Paradee 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.
Ishikawa, Yoshihiro, et al.. (2025). A multifunction murine Col4a1 allele reveals potential gene therapy parameters for Gould syndrome. The Journal of Cell Biology. 224(6). 2 indexed citations
2.
Lesnak, Joseph B., et al.. (2025). Acid-sensing ion channel 3 in macrophages, but not sensory neurons, mediates development of activity-induced muscle pain. Brain Behavior and Immunity. 130. 106122–106122.
3.
4.
Huang, Dake, et al.. (2022). Neuropeptide S (NPS) neurons: Parabrachial identity and novel distributions. The Journal of Comparative Neurology. 530(18). 3157–3178. 10 indexed citations
5.
Coppey, Lawrence J., Alexander Obrosov, Hanna Shevalye, et al.. (2021). Characterization of Mice Ubiquitously Overexpressing Human 15-Lipoxygenase-1: Effect of Diabetes on Peripheral Neuropathy and Treatment with Menhaden Oil. Journal of Diabetes Research. 2021. 1–11. 5 indexed citations
6.
Li, Fengyin, Xin Zhao, Yali Zhang, et al.. (2020). T FH cells depend on Tcf1-intrinsic HDAC activity to suppress CTLA4 and guard B-cell help function. Proceedings of the National Academy of Sciences. 118(2). 26 indexed citations
7.
Xing, Shaojun, Kexin Gai, Xiang Li, et al.. (2019). Tcf1 and Lef1 are required for the immunosuppressive function of regulatory T cells. The Journal of Experimental Medicine. 216(4). 847–866. 72 indexed citations
8.
9.
Paradee, William, et al.. (1999). Fragile X mouse: strain effects of knockout phenotype and evidence suggesting deficient amygdala function. Neuroscience. 94(1). 185–192. 246 indexed citations
10.
Gunter, Chris, William Paradee, Dana C. Crawford, et al.. (1998). Re-examination of factors associated with expansion of CGG repeats using a single nucleotide polymorphism in FMR1. Human Molecular Genetics. 7(12). 1935–1946. 59 indexed citations
11.
Wang, Liang, William Paradee, Chadwick Mullins, et al.. (1997). Aphidicolin-Induced FRA3B Breakpoints Cluster in Two Distinct Regions. Genomics. 41(3). 485–488. 44 indexed citations
12.
Shridhar, Viji, Liang Wang, Rita Rosati, et al.. (1997). Frequent breakpoints in the region surrounding FRA3B in sporadic renal cell carcinomas. Oncogene. 14(11). 1269–1277. 25 indexed citations
13.
Luan, Xudong, et al.. (1997). The FHIT gene is alternatively spliced in normal kidney and renal cell carcinoma. Oncogene. 15(1). 79–86. 20 indexed citations
14.
Paradee, William, Charles M. Wilke, Liang Wang, et al.. (1996). A 350-kb Cosmid Contig in 3p14.2 That Crosses the t(3;8) Hereditary Renal Cell Carcinoma Translocation Breakpoint and 17 Aphidicolin-Induced FRA3B Breakpoints. Genomics. 35(1). 87–93. 48 indexed citations
15.
Shridhar, Ravi, Viji Shridhar, Xiaohong Wang, et al.. (1996). Frequent breakpoints in the 3p14.2 fragile site, FRA3B, in pancreatic tumors.. PubMed. 56(19). 4347–50. 64 indexed citations
16.
17.
Paradee, William, Chadwick Mullins, Thomas W. Glover, et al.. (1995). Precise Localization of Aphidicolin-Induced Breakpoints on the Short Arm of Human Chromosome 3. Genomics. 27(2). 358–361. 39 indexed citations
18.
Paradee, William, Vidya Jayasankar, & Chadwick Mullins. (1994). Molecular characterization of the 3p14.2 constitutive fragile site. The American Journal of Human Genetics. 55. 4 indexed citations
19.
Krebs, Christopher J., Joseph Horton, Chadwick Mullins, William Paradee, & R.T. Taggart. (1993). D11S971 CATT polymorphism (RC27) located near the MEN1 locus at 11q13. Human Molecular Genetics. 2(6). 825–825. 5 indexed citations
20.
Taggart, R.T., et al.. (1993). D11S970 CATT polymorphism (RC29) located near the MEN1 locus at 11q13. Human Molecular Genetics. 2(3). 336–336. 6 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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