Richard Schregle
University of Konstanz
7 Papers
3 Citations
Richard Schregle is an academic researcher from University of Konstanz. The author has contributed to research in topics: Antigen processing & Natural killer T cell. The author has an hindex of 3, co-authored 4 publications.
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Papers
FAT10 localises in dendritic cell aggresome-like induced structures and contributes to their disassembly.
Richard Schregle,Stefanie Mueller,Daniel F. Legler,Jérémie Rossy,Wolfgang A. Krueger,Marcus Groettrup +5 more
TL;DR: It is found that FAT10 localises to DALIS in maturing DCs and that this localisation occurs independently of its conjugation to substrates, which may provide a functional rationale as to why FAT10 is selectively induced upon DC maturation.
FAT10 is phosphorylated by IKKβ to inhibit the antiviral type-I interferon response
Kritika Saxena,N. Roverato,Melody Reithmann,M. Mah,Richard Schregle,Gunter Schmidtke,Ivan Silbern,Henning Urlaub,Annette Aichem +8 more
TL;DR: Strong evidence is provided that FAT10 is phosphorylated by IκB kinase β upon TNF stimulation and during influenza A virus infection on several serine and threonine residues, revealing a mechanism of how phosphorylation of FAT10 limits the production of tissue-destructive IFN-I in inflammation.
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The expression profile of the ubiquitin-like modifier FAT10 in immune cells suggests cell type-specific functions.
Richard Schregle,Mei Min Mah,Stefanie Mueller,Annette Aichem,Michael Basler,Marcus Groettrup +5 more
TL;DR: The findings suggest particular functions of FAT10 in these cell types are suggested and not only a cell type-specific but also a species-specific basal FAT10 expression profile is observed.
The 20S immunoproteasome and constitutive proteasome bind with the same affinity to PA28αβ and equally degrade FAT10
TL;DR: It is concluded that neither differences in the binding strength to, nor activation by PA28αβ, nor a difference in the rate of FAT10-mediated degradation can account for distinct functional capabilities of the IP as compared to the CP.