Claus Scheidereit

17.4k total citations · 4 hit papers
103 papers, 14.3k citations indexed

About

Claus Scheidereit is a scholar working on Cancer Research, Immunology and Molecular Biology. According to data from OpenAlex, Claus Scheidereit has authored 103 papers receiving a total of 14.3k indexed citations (citations by other indexed papers that have themselves been cited), including 71 papers in Cancer Research, 60 papers in Immunology and 54 papers in Molecular Biology. Recurrent topics in Claus Scheidereit's work include NF-κB Signaling Pathways (70 papers), Immune Response and Inflammation (33 papers) and Cytokine Signaling Pathways and Interactions (15 papers). Claus Scheidereit is often cited by papers focused on NF-κB Signaling Pathways (70 papers), Immune Response and Inflammation (33 papers) and Cytokine Signaling Pathways and Interactions (15 papers). Claus Scheidereit collaborates with scholars based in Germany, United States and United Kingdom. Claus Scheidereit's co-authors include Daniel Krappmann, M. Hinz, Miguel Beato, Michael Naumann, F. Gregory Wulczyn, Robert G. Roeder, Bernd Dörken, Eunice N. Hatada, H.M. Westphal and Seda Çöl Arslan and has published in prestigious journals such as Nature, Cell and Proceedings of the National Academy of Sciences.

In The Last Decade

Claus Scheidereit

103 papers receiving 14.0k 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.

NF-κB Function in Growth Control: Regulation of Cyclin D1 Expression and G ₀ /G ₁ -to-S-Phase Transition

1999 689 citations M. Hinz, Daniel Krappmann et al. Molecular and Cellular Biology profile →
Constitutive nuclear factor-kappaB-RelA activation is required for proliferation and survival of Hodgkin's disease tumor cells.

1997 638 citations Florian Emmerich, Daniel Krappmann et al. profile →
IκB kinase complexes: gateways to NF-κB activation and transcription

2006 553 citations Claus Scheidereit profile →
The glucocorticoid receptor binds to defined nucleotide sequences near the promoter of mouse mammary tumour virus

1983 530 citations Claus Scheidereit, H.M. Westphal et al. profile →

Peers — A (Enhanced Table)

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

Name	h						Papers	Cites
Claus Scheidereit Germany	66	7.6k	5.4k	5.3k	2.9k	1.5k	103	14.3k
Yinon Ben‐Neriah Israel	55	10.1k 1.3×	5.9k 1.1×	6.5k 1.2×	4.1k 1.4×	1.2k 0.8×	114	19.1k
Ulrich Siebenlist United States	73	10.6k 1.4×	7.5k 1.4×	10.5k 2.0×	4.3k 1.5×	1.8k 1.2×	176	22.4k
Bing Su United States	59	11.0k 1.4×	3.1k 0.6×	5.6k 1.1×	2.7k 0.9×	1.2k 0.8×	178	17.7k
Harald Wajant Germany	65	8.8k 1.2×	3.8k 0.7×	6.8k 1.3×	2.9k 1.0×	675 0.4×	222	15.6k
Philip N. Tsichlis United States	71	14.4k 1.9×	3.9k 0.7×	4.9k 0.9×	4.6k 1.6×	2.0k 1.3×	196	21.5k
Anning Lin United States	55	10.5k 1.4×	4.0k 0.7×	3.3k 0.6×	2.8k 1.0×	807 0.5×	89	15.5k
Amer A. Beg United States	51	8.0k 1.1×	7.2k 1.3×	8.2k 1.5×	3.5k 1.2×	706 0.5×	95	16.4k
Vincent Bours Belgium	58	5.7k 0.7×	4.4k 0.8×	3.5k 0.7×	2.1k 0.7×	1.0k 0.7×	252	11.9k
Guido Franzoso United States	49	6.5k 0.9×	5.5k 1.0×	5.3k 1.0×	2.7k 0.9×	545 0.4×	96	13.2k
Ranjan Sen United States	49	7.1k 0.9×	3.7k 0.7×	6.5k 1.2×	1.9k 0.7×	1.2k 0.8×	157	13.9k

Countries citing papers authored by Claus Scheidereit

Since Specialization

Citations

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

Fields of papers citing papers by Claus Scheidereit

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Claus Scheidereit

This figure shows the co-authorship network connecting the top 25 collaborators of Claus Scheidereit. A scholar is included among the top collaborators of Claus Scheidereit 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 Claus Scheidereit. Claus Scheidereit 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

Mucka, Patrick, Peter Lindemann, Michael Willenbrock, et al.. (2023). CLK2 and CLK4 are regulators of DNA damage-induced NF-κB targeted by novel small molecule inhibitors. Cell chemical biology. 30(10). 1303–1312.e3. 5 indexed citations

Willenbrock, Michael, et al.. (2023). A computational model of the DNA damage-induced IKK/ NF-κB pathway reveals a critical dependence on irradiation dose and PARP-1. iScience. 26(10). 107917–107917. 3 indexed citations

Lazarow, Katina, et al.. (2022). TSG101 associates with PARP1 and is essential for PARylation and DNA damage‐induced NF‐κB activation. The EMBO Journal. 41(21). e110372–e110372. 25 indexed citations

Klotz, Christian, Séverine Kunz, Marina Kolesnichenko, et al.. (2021). NF-κB determines Paneth versus goblet cell fate decision in the small intestine. Development. 148(21). 11 indexed citations

Kolesnichenko, Marina, Uta E. Höpken, Eva Kärgel, et al.. (2021). Transcriptional repression of NFKBIA triggers constitutive IKK‐ and proteasome‐independent p65/RelA activation in senescence. The EMBO Journal. 40(6). e104296–e104296. 51 indexed citations

Kärgel, Eva, Vedran Franke, Erik McShane, et al.. (2019). Autocrine LTA signaling drives NF-κB and JAK-STAT activity and myeloid gene expression in Hodgkin lymphoma. Blood. 133(13). 1489–1494. 21 indexed citations

Kolesnichenko, Marina, Patrick Beaudette, Oliver Popp, et al.. (2018). The IκB kinase complex is a regulator of mRNA stability. The EMBO Journal. 37(24). 23 indexed citations

Oeckinghaus, Andrea, Elmar Wegener, Uta Ferch, et al.. (2007). Malt1 ubiquitination triggers NF‐κB signaling upon T‐cell activation. The EMBO Journal. 26(22). 4634–4645. 172 indexed citations

Ohazama, Atsushi, Yinling Hu, Ruth Schmidt‐Ullrich, et al.. (2004). A Dual Role for Ikkα in Tooth Development. Developmental Cell. 6(2). 219–227. 61 indexed citations

10.

Slaugenhaupt, Susan A., Anat Blumenfeld, Sandra Gill, et al.. (2001). Tissue-Specific Expression of a Splicing Mutation in the Gene Causes Familial Dysautonomia. The American Journal of Human Genetics. 68(3). 598–605. 448 indexed citations

11.

Krappmann, Daniel, Eunice N. Hatada, Jun Li, et al.. (2000). The IκB Kinase (IKK) Complex Is Tripartite and Contains IKKγ but Not IKAP as a Regular Component. Journal of Biological Chemistry. 275(38). 29779–29787. 97 indexed citations

12.

Hatada, Eunice N., Selina Chen‐Kiang, & Claus Scheidereit. (2000). Interaction and functional interference of C / EBPβ with octamer factors in immunoglobulin gene transcription. European Journal of Immunology. 30(1). 174–184. 16 indexed citations

13.

Emmerich, Florian, Michael Hummel, Gudrun Demel, et al.. (1999). Overexpression of I Kappa B Alpha Without Inhibition of NF-κB Activity and Mutations in the I Kappa B Alpha Gene in Reed-Sternberg Cells. Blood. 94(9). 3129–3134. 19 indexed citations

14.

Hirano, Fuminori, Mirra Chung, Hirotoshi Tanaka, et al.. (1998). Alternative Splicing Variants of IκBβ Establish Differential NF-κB Signal Responsiveness in Human Cells. Molecular and Cellular Biology. 18(5). 2596–2607. 43 indexed citations

15.

Hirano, Fuminori, Hirotoshi Tanaka, Yoshiko Hirano, et al.. (1998). Functional Interference of Sp1 and NF-κB through the Same DNA Binding Site. Molecular and Cellular Biology. 18(3). 1266–1274. 142 indexed citations

16.

Brüggemeier, Ulf, Martha Kalff, Sabine Franke, Claus Scheidereit, & Miguel Beato. (1991). Ubiquitous transcription factor OTF-1 mediates induction of the MMTV promoter through synergistic interaction with hormone receptors. Cell. 64(3). 565–572. 197 indexed citations

17.

Scheidereit, Claus, et al.. (1991). Neither the endogenous nor a functional steroid hormone receptor binding site transactivate the ribosomal RNA gene promoter in vitro. The Journal of Steroid Biochemistry and Molecular Biology. 39(4). 409–418. 7 indexed citations

18.

Scheidereit, Claus, Dietmar von der Ahe, Andrew C.B. Cato, et al.. (1989). Protein-DNA Interactions at Steroid Hormone Regulated Genes. Endocrine Research. 15(4). 417–440. 15 indexed citations

19.

Scheidereit, Claus, H.M. Westphal, Christopher Carlson, H.E. Bosshard, & Miguel Beato. (1986). Molecular Model of the Interaction Between the Glucocorticoid Receptor and the Regulatory Elements of Inducible Genes. DNA. 5(5). 383–391. 95 indexed citations

20.

Scheidereit, Claus, Dietmar von der Ahe, Andrew C.B. Cato, et al.. (1986). Mechanism of gene regulation by steroid hormones. Journal of Steroid Biochemistry. 24(1). 19–24. 34 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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