Axel Witt

647 total citations
11 papers, 464 citations indexed

About

Axel Witt is a scholar working on Molecular Biology, Immunology and Cancer Research. According to data from OpenAlex, Axel Witt has authored 11 papers receiving a total of 464 indexed citations (citations by other indexed papers that have themselves been cited), including 11 papers in Molecular Biology, 5 papers in Immunology and 4 papers in Cancer Research. Recurrent topics in Axel Witt's work include Ubiquitin and proteasome pathways (3 papers), interferon and immune responses (2 papers) and Cell death mechanisms and regulation (2 papers). Axel Witt is often cited by papers focused on Ubiquitin and proteasome pathways (3 papers), interferon and immune responses (2 papers) and Cell death mechanisms and regulation (2 papers). Axel Witt collaborates with scholars based in Germany, United States and France. Axel Witt's co-authors include Domagoj Vucic, Hamid Kashkar, Martin Krönke, Kerstin Brinkmann, Liping Zhao, John A. Mercer, David William Provance, Oliver Coutelle, Martin Bähler and Jens M. Seeger and has published in prestigious journals such as Proceedings of the National Academy of Sciences, Nature Communications and Cell Death and Differentiation.

In The Last Decade

Axel Witt

11 papers receiving 459 citations

Peers

Axel Witt
Shengyong Yang China
Zhifang Hao China
Dianhong Luo United States
И. В. Кондакова Russia
Mélanie Lambert France
Aktar Ali United States
Vinay Kumar Rao Singapore
Hiroyuki Kunimoto Japan
Elena Kotsaki Greece
Leyuan Bao China
Shengyong Yang China
Axel Witt
Citations per year, relative to Axel Witt Axel Witt (= 1×) peers Shengyong Yang

Countries citing papers authored by Axel Witt

Since Specialization
Citations

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

Fields of papers citing papers by Axel Witt

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Axel Witt

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

All Works

11 of 11 papers shown
1.
Goncharov, Tatiana, László G. Kömüves, Matthias Kist, et al.. (2024). Simultaneous substrate and ubiquitin modification recognition by bispecific antibodies enables detection of ubiquitinated RIP1 and RIP2. Science Signaling. 17(819). eabn1101–eabn1101. 1 indexed citations
2.
Witt, Axel, Tatiana Goncharov, Matthias Kist, et al.. (2023). XIAP deletion sensitizes mice to TNF-induced and RIP1-mediated death. Cell Death and Disease. 14(4). 262–262. 5 indexed citations
3.
Schiffmann, Lars M., Melanie Fritsch, Saskia Diana Günther, et al.. (2020). Mitochondrial respiration controls neoangiogenesis during wound healing and tumour growth. Nature Communications. 11(1). 53 indexed citations
4.
Holliday, Michael, Axel Witt, Alejandro Rodríguez Gama, et al.. (2019). Structures of autoinhibited and polymerized forms of CARD9 reveal mechanisms of CARD9 and CARD11 activation. Nature Communications. 10(1). 26 indexed citations
5.
Witt, Axel & Domagoj Vucic. (2017). Diverse ubiquitin linkages regulate RIP kinases-mediated inflammatory and cell death signaling. Cell Death and Differentiation. 24(7). 1160–1171. 100 indexed citations
6.
Witt, Axel, Jens M. Seeger, Oliver Coutelle, et al.. (2015). IAP antagonization promotes inflammatory destruction of vascular endothelium. EMBO Reports. 16(6). 719–727. 12 indexed citations
7.
Günther, Saskia Diana, Susanne Brodesser, Katja Wiegmann, et al.. (2015). Cytochrome c oxidase deficiency accelerates mitochondrial apoptosis by activating ceramide synthase 6. Cell Death and Disease. 6(3). e1691–e1691. 58 indexed citations
8.
Coutelle, Oliver, Hue‐Tran Hornig‐Do, Axel Witt, et al.. (2014). Embelin inhibits endothelial mitochondrial respiration and impairs neoangiogenesis during tumor growth and wound healing. EMBO Molecular Medicine. 6(5). 624–639. 65 indexed citations
9.
Brinkmann, Kerstin, Paola Zigrino, Axel Witt, et al.. (2013). Ubiquitin C-Terminal Hydrolase-L1 Potentiates Cancer Chemosensitivity by Stabilizing NOXA. Cell Reports. 3(3). 881–891. 62 indexed citations
10.
Witt, Axel, Hans-Juergen Ahr, Susanne Brendler‐Schwaab, Harald Enzmann, & Wolfram Steinke. (1998). Carcinogen-induced Mitochondrial DNA Damage in the In Ovo Model. Toxicology in Vitro. 12(3). 329–333. 6 indexed citations
11.
Zhao, Liping, et al.. (1996). Cloning and characterization of myr 6, an unconventional myosin of the dilute/myosin-V family.. Proceedings of the National Academy of Sciences. 93(20). 10826–10831. 76 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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