SIAH ubiquitin E3 ligases as modulators of inflammatory gene expression

Schmitz, Lienhard; Dreute, Jan; Pfisterer, Maximilian; Guenther, Stefan; Kracht, Michael; Chillappagari, Shashipavan

doi:10.1016/j.heliyon.2022.e09029

Item

ITEM ACTIONSEXPORT

Add to Basket

Local TagsRelease HistoryDetailsSummary

Released

Journal Article

SIAH ubiquitin E3 ligases as modulators of inflammatory gene expression

MPS-Authors

/persons/resource/persons224128

Guenther, Stefan
Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society;

External Resource

No external resources are shared

Fulltext (restricted access)

There are currently no full texts shared for your IP range.

Fulltext (public)

There are no public fulltexts stored in PuRe

Supplementary Material (public)

There is no public supplementary material available

Citation

Schmitz, L., Dreute, J., Pfisterer, M., Guenther, S., Kracht, M., & Chillappagari, S. (2022). SIAH ubiquitin E3 ligases as modulators of inflammatory gene expression. HELIYON, 8(3): e09029. doi:10.1016/j.heliyon.2022.e09029.

Cite as: https://hdl.handle.net/21.11116/0000-000A-ACEF-8

Abstract

The functionally redundant ubiquitin E3 ligases SIAH1 and SIAH2 have been implicated in the regulation of metabolism and the hypoxic response, while their role in other signal-mediated processes such inflammatory gene expression remains to be defined. Here we have downregulated the expression of both SIAH proteins with specific siRNAs and investigated the functional consequences for IL-1 alpha-induced gene expression. The knockdown of SIAH1/2 modulated the expression of approximately one third of IL-1 alpha-regulated genes. These effects were not due to changes in the NF-kappa B and MAPK signaling pathways and rather employed further processes including those mediated by the coactivator p300. Most of the proteins encoded by SIAH1/2-regulated genes form a regulatory network of proinflammatory factors. Thus SIAH1/2 proteins function as variable rheostats that control the amplitude rather than the principal activation of the inflammatory gene response.