Recombinant Rat E3 ubiquitin-protein ligase RNF152 (Rnf152)

General Information

Recombinant Rat E3 ubiquitin-protein ligase RNF152 (Rnf152), also known as Ring finger protein 152, is an E3 ubiquitin ligase containing a RING domain and a transmembrane (TM) domain . In humans, the gene that encodes this protein is named RNF152 . RNF152 participates in different signaling pathways and cellular processes .

Gene Information

Function and Mechanism

RNF152 functions as an E3 ubiquitin ligase, which mediates the transfer of ubiquitin to target proteins, influencing their stability, function, or localization. RNF152 is involved in:

• Regulation of inflammatory response RNF152 positively regulates TLR/IL-1R-mediated inflammatory response by facilitating oligomerization of MyD88, which subsequently promotes the assembly of Myddosome . RNF152 is essential for TLR/IL-1R-mediated, MyD88-dependent signal transduction .

• Regulation of mTORC1 signaling RNF152 acts as a negative regulator of mTORC1 signaling by mediating ubiquitination of RagA/RRAGA and RHEB .

• Regulation of TLR/IL-1R signaling RNF152 positively regulates TLR/IL-1R signaling by enhancing MyD88 oligomerization .

RNF152 has been identified as a regulator of IL-1β signaling through screening of human cDNA expression clones . Overexpression of RNF152 can activate the NF-κB reporter in a dose-dependent manner and enhance IL-1β-triggered NF-κB activation . It also enhances the transcription of inflammatory cytokines induced by IL-1β .

RNF152 and Inflammatory Response

RNF152 plays a role in MyD88-dependent signaling pathways, which are crucial for the inflammatory response . Studies using RNF152-deficient mice have shown that RNF152 is required for IL-1R-, TLR2-, and TLR4-mediated signaling, but not TLR3-mediated signaling .

Experiments have demonstrated that RNF152-deficient mice produce fewer inflammatory cytokines in response to LPS and are more resistant to LPS-induced lethal endotoxemia . The production of IL-6 and TNFα induced by LPS was significantly decreased in RNF152-deficient mice, whereas IFN-β production, which is mediated by TRIF-dependent signaling, was not affected .

RNF152 and Disease

• Endotoxemia RNF152-deficient mice exhibit delayed onset of death and reduced lethality compared to wild-type mice after LPS challenge, suggesting RNF152's role in TLR/IL-1R-mediated inflammatory responses .

• Cancer RNF152 expression and function in cancer are not well-documented in the provided. Further research may be needed to elucidate its specific involvement in cancer development or progression .

• Other diseases RNF152 may play a role in additional diseases or conditions, but this is not detailed in the provided. Further studies could explore its involvement in other pathological states .