Thomas W. Bebee

876 total citations
16 papers, 619 citations indexed

About

Thomas W. Bebee is a scholar working on Molecular Biology, Genetics and Cancer Research. According to data from OpenAlex, Thomas W. Bebee has authored 16 papers receiving a total of 619 indexed citations (citations by other indexed papers that have themselves been cited), including 16 papers in Molecular Biology, 5 papers in Genetics and 3 papers in Cancer Research. Recurrent topics in Thomas W. Bebee's work include RNA Research and Splicing (11 papers), RNA modifications and cancer (10 papers) and Neurogenetic and Muscular Disorders Research (5 papers). Thomas W. Bebee is often cited by papers focused on RNA Research and Splicing (11 papers), RNA modifications and cancer (10 papers) and Neurogenetic and Muscular Disorders Research (5 papers). Thomas W. Bebee collaborates with scholars based in United States and China. Thomas W. Bebee's co-authors include Russ P. Carstens, Dawn S. Chandler, Juw Won Park, Yi Xing, Benjamin Cieply, Claude C. Warzecha, Catherine Dominguez, Yang Guo, Xuequn Shang and Yueqin Yang and has published in prestigious journals such as Journal of Biological Chemistry, Nature Communications and PLoS ONE.

In The Last Decade

Thomas W. Bebee

16 papers receiving 613 citations

Peers — A (Enhanced Table)

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

Name	h						Papers	Cites
Thomas W. Bebee United States	14	537	143	108	53	45	16	619
Erin L. Wuebben United States	8	380 0.7×	131 0.9×	30 0.3×	149 2.8×	53 1.2×	8	486
Henrikki Almusa Finland	11	284 0.5×	120 0.8×	54 0.5×	70 1.3×	123 2.7×	31	508
Oriana Romano Italy	12	349 0.6×	46 0.3×	151 1.4×	49 0.9×	68 1.5×	21	542
Ana Hidalgo‐Sastre Germany	11	300 0.6×	59 0.4×	21 0.2×	123 2.3×	82 1.8×	14	444
Simona Pedrotti Italy	11	661 1.2×	218 1.5×	78 0.7×	56 1.1×	44 1.0×	14	746
Ji Yoo Kim Japan	9	321 0.6×	32 0.2×	29 0.3×	37 0.7×	62 1.4×	13	446
Yu Gyoung Tak United States	6	378 0.7×	95 0.7×	28 0.3×	32 0.6×	151 3.4×	6	509
Alex Kreig United States	4	415 0.8×	79 0.6×	68 0.6×	82 1.5×	33 0.7×	6	548
Dave P. Witte United States	8	233 0.4×	101 0.7×	19 0.2×	51 1.0×	45 1.0×	10	390
Ronny Derks Netherlands	10	221 0.4×	40 0.3×	31 0.3×	19 0.4×	130 2.9×	15	326

Countries citing papers authored by Thomas W. Bebee

Since Specialization

Citations

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

Fields of papers citing papers by Thomas W. Bebee

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Thomas W. Bebee. 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 Thomas W. Bebee. The network helps show where Thomas W. Bebee may publish in the future.

Co-authorship network of co-authors of Thomas W. Bebee

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

All Works

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16 of 16 papers shown

Bebee, Thomas W., Caleb M. Radens, Chris McDermott‐Roe, et al.. (2017). ESRP1 Mutations Cause Hearing Loss due to Defects in Alternative Splicing that Disrupt Cochlear Development. Developmental Cell. 43(3). 318–331.e5. 41 indexed citations

Comiskey, Daniel F., Aishwarya G. Jacob, Thomas W. Bebee, et al.. (2017). A novel mouse model of rhabdomyosarcoma underscores the dichotomy of MDM2-ALT1 function in vivo. Oncogene. 37(1). 95–106. 10 indexed citations

Cieply, Benjamin, Juw Won Park, Angela Nakauka‐Ddamba, et al.. (2016). Multiphasic and Dynamic Changes in Alternative Splicing during Induction of Pluripotency Are Coordinated by Numerous RNA-Binding Proteins. Cell Reports. 15(2). 247–255. 56 indexed citations

Bebee, Thomas W., Sunder Sims‐Lucas, Juw Won Park, et al.. (2016). Ablation of the epithelial‐specific splicing factor Esrp1 results in ureteric branching defects and reduced nephron number. Developmental Dynamics. 245(10). 991–1000. 16 indexed citations

Yang, Yueqin, Juw Won Park, Thomas W. Bebee, et al.. (2016). Determination of a Comprehensive Alternative Splicing Regulatory Network and Combinatorial Regulation by Key Factors during the Epithelial-to-Mesenchymal Transition. Molecular and Cellular Biology. 36(11). 1704–1719. 101 indexed citations

Bhate, Amruta, Darren J. Parker, Thomas W. Bebee, et al.. (2015). ESRP2 controls an adult splicing programme in hepatocytes to support postnatal liver maturation. Nature Communications. 6(1). 8768–8768. 78 indexed citations

Bebee, Thomas W., Juw Won Park, Claude C. Warzecha, et al.. (2015). The splicing regulators Esrp1 and Esrp2 direct an epithelial splicing program essential for mammalian development. eLife. 4. 106 indexed citations

Jacob, Aishwarya G., Ravi K. Singh, Daniel F. Comiskey, et al.. (2014). Stress-Induced Alternative Splice Forms of MDM2 and MDMX Modulate the p53-Pathway in Distinct Ways. PLoS ONE. 9(8). e104444–e104444. 21 indexed citations

Jacob, Aishwarya G., Ravi K. Singh, Fuad Mohammad, Thomas W. Bebee, & Dawn S. Chandler. (2014). The Splicing Factor FUBP1 Is Required for the Efficient Splicing of Oncogene MDM2 Pre-mRNA. Journal of Biological Chemistry. 289(25). 17350–17364. 32 indexed citations

10.

Bebee, Thomas W., Benjamin Cieply, & Russ P. Carstens. (2014). Genome-Wide Activities of RNA Binding Proteins That Regulate Cellular Changes in the Epithelial to Mesenchymal Transition (EMT). Advances in experimental medicine and biology. 825. 267–302. 19 indexed citations

11.

Bebee, Thomas W., et al.. (2012). Hypoxia is a modifier of SMN2 splicing and disease severity in a severe SMA mouse model. Human Molecular Genetics. 21(19). 4301–4313. 23 indexed citations

12.

Bebee, Thomas W., Catherine Dominguez, & Dawn S. Chandler. (2012). Mouse models of SMA: tools for disease characterization and therapeutic development. Human Genetics. 131(8). 1277–1293. 46 indexed citations

13.

Bebee, Thomas W., Jordan T. Gladman, & Dawn S. Chandler. (2011). Generation of a tamoxifen inducible SMN mouse for temporal SMN replacement. genesis. 49(12). 927–934. 1 indexed citations

14.

Gladman, Jordan T., Thomas W. Bebee, Xueyong Wang, et al.. (2010). A humanized Smn gene containing the SMN2 nucleotide alteration in exon 7 mimics SMN2 splicing and the SMA disease phenotype. Human Molecular Genetics. 19(21). 4239–4252. 23 indexed citations

15.

Bebee, Thomas W.. (2010). Splicing regulation of the Survival Motor Neuron genes and implications for treatment of spinal muscular atrophy. Frontiers in bioscience. 15(1). 1191–1191. 30 indexed citations

16.

Singh, Ravi K., et al.. (2009). Conserved sequences in the final intron of MDM2 are essential for the regulation of alternative splicing of MDM2 in response to stress. Experimental Cell Research. 315(19). 3419–3432. 16 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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