Thomas Quast

3.3k total citations
28 papers, 1.4k citations indexed

About

Thomas Quast is a scholar working on Immunology, Molecular Biology and Cell Biology. According to data from OpenAlex, Thomas Quast has authored 28 papers receiving a total of 1.4k indexed citations (citations by other indexed papers that have themselves been cited), including 18 papers in Immunology, 9 papers in Molecular Biology and 9 papers in Cell Biology. Recurrent topics in Thomas Quast's work include Immunotherapy and Immune Responses (13 papers), T-cell and B-cell Immunology (8 papers) and Immune Cell Function and Interaction (4 papers). Thomas Quast is often cited by papers focused on Immunotherapy and Immune Responses (13 papers), T-cell and B-cell Immunology (8 papers) and Immune Cell Function and Interaction (4 papers). Thomas Quast collaborates with scholars based in Germany, United States and Australia. Thomas Quast's co-authors include Waldemar Kolanus, Christian Kurts, Volker Herzog, Waldemar Kolanus, Irmgard Förster, Michael Famulok, Elisabeth Kremmer, Seergazhi G. Srivatsan, Inga Bauer and Anton Schmitz and has published in prestigious journals such as Nature, Proceedings of the National Academy of Sciences and The Journal of Cell Biology.

In The Last Decade

Thomas Quast

27 papers receiving 1.4k citations

Peers

Thomas Quast
Sharmila Masli United States
Yee-Guide Yeung United States
Janelle Waite United States
Allison L. Bayer United States
Michael W. Olszowy United States
Oskar Laur United States
Sharmila Masli United States
Thomas Quast
Citations per year, relative to Thomas Quast Thomas Quast (= 1×) peers Sharmila Masli

Countries citing papers authored by Thomas Quast

Since Specialization
Citations

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

Fields of papers citing papers by Thomas Quast

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Thomas Quast

This figure shows the co-authorship network connecting the top 25 collaborators of Thomas Quast. A scholar is included among the top collaborators of Thomas Quast 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 Quast. Thomas Quast 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.
Müller, Linda, Bettina Jux, Susanne V. Schmidt, et al.. (2024). Differential impact of high-salt levels in vitro and in vivo on macrophage core functions. Molecular Biology Reports. 51(1). 343–343. 2 indexed citations
2.
Hauschild, Robert, Lili Zhang, Thomas Quast, et al.. (2022). Multiple centrosomes enhance migration and immune cell effector functions of mature dendritic cells. The Journal of Cell Biology. 221(12). 13 indexed citations
3.
Quast, Thomas, et al.. (2022). A Stable Chemokine Gradient Controls Directional Persistence of Migrating Dendritic Cells. Frontiers in Cell and Developmental Biology. 10. 943041–943041. 7 indexed citations
4.
Popović, Zoran V., Maria Embgenbroich, Viola Nordström, et al.. (2017). Hyperosmolarity impedes the cross-priming competence of dendritic cells in a TRIF-dependent manner. Scientific Reports. 7(1). 311–311. 12 indexed citations
5.
Quast, Thomas, et al.. (2017). Dynamin2 controls Rap1 activation and integrin clustering in human T lymphocyte adhesion. PLoS ONE. 12(3). e0172443–e0172443. 9 indexed citations
6.
Eickhoff, Sarah, Thomas Quast, Sammy Bedoui, et al.. (2017). CD8+ T Cells Orchestrate pDC-XCR1+ Dendritic Cell Spatial and Functional Cooperativity to Optimize Priming. Immunity. 46(2). 205–219. 254 indexed citations
7.
Rudolph, Janna, Annkristin Heine, Thomas Quast, et al.. (2015). The JAK Inhibitor Ruxolitinib Impairs Dendritic Cell Migration Via Off-Target Inhibition of Rock. Blood. 126(23). 3423–3423. 1 indexed citations
8.
Quast, Thomas, Agnes Schröder, Stephanie Hucke, et al.. (2013). Salt-Dependent Chemotaxis of Macrophages. PLoS ONE. 8(9). e73439–e73439. 63 indexed citations
9.
Quast, Thomas, Yahya Homsi, Shoshana Levy, et al.. (2011). CD81 is essential for the formation of membrane protrusions and regulates Rac1-activation in adhesion-dependent immune cell migration. Blood. 118(7). 1818–1827. 58 indexed citations
10.
Lukacs‐Kornek, Veronika, Christoph A. Thaiss, Thomas Quast, et al.. (2010). Alternative cross-priming through CCL17-CCR4-mediated attraction of CTLs toward NKT cell–licensed DCs. Nature Immunology. 11(4). 313–320. 182 indexed citations
11.
Stutte, Susanne, Thomas Quast, Terhi Savinko, et al.. (2010). Requirement of CCL17 for CCR7- and CXCR4-dependent migration of cutaneous dendritic cells. Proceedings of the National Academy of Sciences. 107(19). 8736–8741. 94 indexed citations
12.
Quast, Thomas, Niklas Czeloth, Reinhold Förster, et al.. (2009). Cytohesin-1 controls the activation of RhoA and modulates integrin-dependent adhesion and migration of dendritic cells. Blood. 113(23). 5801–5810. 51 indexed citations
13.
Quast, Thomas, Sascha Keller, Waldemar Kolanus, et al.. (2008). Transfer of T Cell Surface Molecules to Dendritic Cells upon CD4+ T Cell Priming Involves Two Distinct Mechanisms. The Journal of Immunology. 181(6). 3965–3973. 26 indexed citations
14.
Quast, Thomas, Christiane Kummer, Sven Wehner, et al.. (2006). Keratinocytes from APP/APLP2-deficient mice are impaired in proliferation, adhesion and migration in vitro. Experimental Cell Research. 312(11). 1939–1949. 30 indexed citations
15.
Hafner, Markus, Anton Schmitz, Seergazhi G. Srivatsan, et al.. (2006). Inhibition of cytohesins by SecinH3 leads to hepatic insulin resistance. Nature. 444(7121). 941–944. 206 indexed citations
16.
Quast, Thomas, et al.. (2004). Normalized Proliferation of Normal and Psoriatic Keratinocytes by Suppression of sAPPα-Release. Journal of Investigative Dermatology. 123(3). 556–563. 20 indexed citations
17.
Quast, Thomas, et al.. (2004). Simultaneous cell death and desquamation of the embryonic diffusion barrier during epidermal development. Experimental Cell Research. 299(2). 415–426. 25 indexed citations
18.
Quast, Thomas, et al.. (2003). sAPP as a regulator of dendrite motility and melanin release in epidermal melanocytes and melanoma cells. The FASEB Journal. 17(12). 1739–1741. 27 indexed citations
19.
Kummer, Christiane, Sven Wehner, Thomas Quast, Sabine Werner, & Volker Herzog. (2002). Expression and Potential Function of β-Amyloid Precursor Proteins during Cutaneous Wound Repair. Experimental Cell Research. 280(2). 222–232. 37 indexed citations
20.
Quast, Thomas, et al.. (1996). <title>Flat panel display test and evaluation for U.S. military applications</title>. Proceedings of SPIE, the International Society for Optical Engineering/Proceedings of SPIE. 2734. 304–310. 1 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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