Thomas Maciag

8.9k total citations · 2 hit papers
63 papers, 7.3k citations indexed

About

Thomas Maciag is a scholar working on Molecular Biology, Cell Biology and Cancer Research. According to data from OpenAlex, Thomas Maciag has authored 63 papers receiving a total of 7.3k indexed citations (citations by other indexed papers that have themselves been cited), including 54 papers in Molecular Biology, 18 papers in Cell Biology and 11 papers in Cancer Research. Recurrent topics in Thomas Maciag's work include Fibroblast Growth Factor Research (24 papers), Cell Adhesion Molecules Research (10 papers) and S100 Proteins and Annexins (9 papers). Thomas Maciag is often cited by papers focused on Fibroblast Growth Factor Research (24 papers), Cell Adhesion Molecules Research (10 papers) and S100 Proteins and Annexins (9 papers). Thomas Maciag collaborates with scholars based in United States, Italy and Australia. Thomas Maciag's co-authors include Wilson H. Burgess, Robert Friesel, Igor Prudovsky, Francesca Tarantini, Jeanette A.M. Maier, Anthony Jackson, Raffaella Soldi, Stephen Bellum, Pamela J. Voulalas and Tevie Mehlman and has published in prestigious journals such as Nature, Science and Proceedings of the National Academy of Sciences.

In The Last Decade

Thomas Maciag

63 papers receiving 7.1k citations

Hit Papers

align trajectories

What are hit papers?

Hit papers significantly outperform the citation benchmark for their cohort. A paper qualifies if it has ≥500 total citations, achieves ≥1.5× the top-1% citation threshold for papers in the same subfield and year (this is the minimum needed to enter the top 1%, not the average within it), or reaches the top citation threshold in at least one of its specific research topics.

THE HEPARIN-BINDING (FIBROBLAST) GROWTH FACTOR FAMILY OF PROTEINS

1989 1.7k citations Wilson H. Burgess, Thomas Maciag Annual Review of Biochemistry profile →
Human Endothelial Cell Growth Factor: Cloning, Nucleotide Sequence, and Chromosome Localization

1986 586 citations Michael Jaye, Wilson H. Burgess et al. Science profile →

Peers — A (Enhanced Table)

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

Name	h						Papers	Cites
Thomas Maciag United States	37	5.3k	1.9k	1.0k	824	741	63	7.3k
Åke Wasteson Sweden	40	4.5k 0.8×	2.2k 1.2×	934 0.9×	826 1.0×	1.0k 1.4×	88	7.6k
Robert Friesel United States	40	4.5k 0.8×	1.5k 0.8×	907 0.9×	531 0.6×	844 1.1×	85	6.2k
Jung San Huang United States	38	4.1k 0.8×	1.0k 0.5×	1.1k 1.1×	817 1.0×	1.2k 1.7×	93	7.3k
Gregory David United States	48	4.5k 0.8×	2.4k 1.2×	751 0.7×	641 0.8×	799 1.1×	107	7.0k
Takashi Muramatsu Japan	47	4.2k 0.8×	4.0k 2.1×	849 0.8×	641 0.8×	843 1.1×	156	6.9k
Shintaro Nomura Japan	41	3.8k 0.7×	1.2k 0.6×	743 0.7×	1.3k 1.6×	1.3k 1.8×	128	7.7k
Masayuki Ozawa Japan	44	6.2k 1.2×	2.4k 1.3×	368 0.4×	905 1.1×	889 1.2×	133	8.4k
Toru Miki United States	37	6.6k 1.2×	2.8k 1.5×	775 0.8×	957 1.2×	2.0k 2.6×	77	9.2k
Robert G. Oshima United States	51	4.4k 0.8×	2.7k 1.4×	502 0.5×	762 0.9×	961 1.3×	119	7.5k
Joachim Sasse United States	36	3.7k 0.7×	1.7k 0.9×	839 0.8×	301 0.4×	499 0.7×	71	5.5k

Countries citing papers authored by Thomas Maciag

Since Specialization

Citations

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

Fields of papers citing papers by Thomas Maciag

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Thomas Maciag

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

All Works

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20 of 20 papers shown

Duarte, Maria F., Vihren N. Kolev, Doreen Kacer, et al.. (2008). Novel Cross-Talk between Three Cardiovascular Regulators: Thrombin Cleavage Fragment of Jagged1 Induces Fibroblast Growth Factor 1 Expression and Release. Molecular Biology of the Cell. 19(11). 4863–4874. 17 indexed citations

Soldi, Raffaella, Anna Mandinova, Krishnan Venkataraman, et al.. (2007). Sphingosine kinase 1 is a critical component of the copper-dependent FGF1 export pathway. Experimental Cell Research. 313(15). 3308–3318. 24 indexed citations

Kolev, Vihren N., Doreen Kacer, Radiana Trifonova, et al.. (2005). The intracellular domain of Notch ligand Delta1 induces cell growth arrest. FEBS Letters. 579(25). 5798–5802. 36 indexed citations

Trifonova, Radiana, Deena Small, Doreen Kacer, et al.. (2004). The Non-transmembrane Form of Delta1, but Not of Jagged1, Induces Normal Migratory Behavior Accompanied by Fibroblast Growth Factor Receptor 1-dependent Transformation. Journal of Biological Chemistry. 279(14). 13285–13288. 30 indexed citations

Small, Deena, Д. В. Коваленко, Raffaella Soldi, et al.. (2003). Notch Activation Suppresses Fibroblast Growth Factor-dependent Cellular Transformation. Journal of Biological Chemistry. 278(18). 16405–16413. 54 indexed citations

Landriscina, Matteo, Raffaella Soldi, Cinzia Bagalá, et al.. (2001). S100A13 Participates in the Release of Fibroblast Growth Factor 1 in Response to Heat Shock in Vitro. Journal of Biological Chemistry. 276(25). 22544–22552. 70 indexed citations

Lindner, Volkhard, et al.. (2001). Members of the Jagged/Notch Gene Families Are Expressed in Injured Arteries and Regulate Cell Phenotype via Alterations in Cell Matrix and Cell-Cell Interaction. American Journal Of Pathology. 159(3). 875–883. 152 indexed citations

Carreira, Carla Mouta, et al.. (2001). The Comparative Release of FGF1 by Hypoxia and Temperature Stress. Growth Factors. 18(4). 277–285. 44 indexed citations

Tarantini, Francesca, Theresa LaVallee, Anthony Jackson, et al.. (1998). The Extravesicular Domain of Synaptotagmin-1 Is Released with the Latent Fibroblast Growth Factor-1 Homodimer in Response to Heat Shock. Journal of Biological Chemistry. 273(35). 22209–22216. 62 indexed citations

10.

Carreira, Carla Mouta, Theresa LaVallee, Francesca Tarantini, et al.. (1998). S100A13 Is Involved in the Regulation of Fibroblast Growth Factor-1 and p40 Synaptotagmin-1 Release in Vitro. Journal of Biological Chemistry. 273(35). 22224–22231. 102 indexed citations

11.

Finch, Paul W., Lorrin Yee, Ming Chu, et al.. (1997). Inhibition of Growth Factor Mitogenicity and Growth of Tumor Cell Xenografts by a Sulfonated Distamycin A Derivative. Pharmacology. 55(6). 269–278. 10 indexed citations

12.

Zimrin, Ann B., Michael S. Pepper, Grainne A. McMahon, et al.. (1996). An Antisense Oligonucleotide to the Notch Ligand Jagged Enhances Fibroblast Growth Factor-induced Angiogenesis in Vitro. Journal of Biological Chemistry. 271(51). 32499–32502. 122 indexed citations

13.

Hla, Timothy, et al.. (1995). Characterization of edg-2, a human homologue of theXenopus maternal transcript G10 from endothelial cells. Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression. 1260(2). 227–229. 20 indexed citations

14.

Imamura, Toru, Stanley Friedman, Susan Gamble, et al.. (1995). Identification of the domain within fibroblast growth factor-1 responsible for heparin-dependence. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research. 1266(2). 124–130. 14 indexed citations

15.

Forough, Reza, Kurt A. Engleka, John A. Thompson, et al.. (1991). Differential expression in Escherichia coli of the α and β forms of heparin-binding acidic fibroblast growth factor-1: potential role of RNA secondary structure. Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression. 1090(3). 293–298. 40 indexed citations

16.

Burgess, Wilson H. & Thomas Maciag. (1989). THE HEPARIN-BINDING (FIBROBLAST) GROWTH FACTOR FAMILY OF PROTEINS. Annual Review of Biochemistry. 58(1). 575–602. 1662 indexed citations breakdown →

17.

Rosengart, Todd K., John P. Kupferschmid, Victor J. Ferrans, et al.. (1988). Heparin-binding growth factor-I (endothelial cell growth factor) binds to endothelium in vivo. Journal of Vascular Surgery. 7(2). 311–317. 23 indexed citations

18.

Rosengart, Todd K., Warren V. Johnson, Robert Friesel, Richard E. Clark, & Thomas Maciag. (1988). Heparin protects heparin-binding growth factor-I from proteolytic inactivation in vitro. Biochemical and Biophysical Research Communications. 152(1). 432–440. 126 indexed citations

19.

Wu, Doris K., Thomas Maciag, & Jean de Vellis. (1988). Regulation of neuroblast proliferation by hormones and growth factors in chemically defined medium. Journal of Cellular Physiology. 136(2). 367–372. 28 indexed citations

20.

Jaye, Michael, et al.. (1985). Modulation of the sis Gene Transcript During Endothelial Cell Differentiation in Vitro. Science. 228(4701). 882–885. 104 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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