A super-enhancer maintains homeostatic expression of Regnase-1

Yang, Riyun; Wu, Yuanyuan; Ming, Yue; Xu, Yuanpei; Wang, Shouyan; Shen, Jianbo; Wang, Chenlu; Xia, Chen; Wang, Yongming; Mao, Renfang; Fan, Yihui

doi:10.1016/j.gene.2018.05.052

Cited by 5 publications

(4 citation statements)

References 23 publications

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“…The information regarding epiCRISPR vector was published previously (Yang et al, 2018). We constructed sgPD-L1-1, sgPD-L1-2, sgPD-L1-3, sgPD-L1-4 by ligation and digestion.…”

Section: Methods Details Plasmidsmentioning

confidence: 99%

A Tumor-Specific Super-Enhancer Drives Immune Evasion by Guiding Synchronous Expression of PD-L1 and PD-L2

Zhang

et al. 2019

Cell Reports

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“…The information regarding epiCRISPR vector was published previously (Yang et al, 2018). We constructed sgPD-L1-1, sgPD-L1-2, sgPD-L1-3, sgPD-L1-4 by ligation and digestion.…”

Section: Methods Details Plasmidsmentioning

confidence: 99%

A Tumor-Specific Super-Enhancer Drives Immune Evasion by Guiding Synchronous Expression of PD-L1 and PD-L2

Zhang

et al. 2019

Cell Reports

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“…Therefore, we determined whether QKI expression is regulated by SE. We used a small molecule named JQ1, which can specifically disrupt SE (23). Luciferase assay showed that JQ1 could significantly reduce the pGL3 luciferase reporter luciferase activity that contained YY1 motif (Fig.…”

Section: Yy1 Enhances Qki Gene Transcription and Translation Dependinmentioning

confidence: 99%

YY1 Complex Promotes Quaking Expression via Super-Enhancer Binding during EMT of Hepatocellular Carcinoma

et al. 2019

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Quaking (QKI) is an alternative splicing factor that can regulate circRNA formation in the progression of epithelialmesenchymal transition, but the mechanism remains unclear. High expression of QKI is correlated with short survival time, metastasis, and high clinical stage and pathology grade in hepatocellular carcinoma (HCC). Here we report that transcription of the QKI gene was activated by the Yin-Yang 1 (YY1)/p65/p300 complex, in which YY1 bound to the superenhancer and promoter of QKI, p65 combined with the promoter, and p300 served as a mediator to maintain the stability of the complex. This YY1/p65/p300 complex increased QKI expression to promote the malignancy of HCC as well as an increased circRNA formation in vitro and in vivo. Hyperoside is one of several plant-derived flavonol glycoside compounds. Through virtual screening and antitumor activity analysis, we found that hyperoside inhibited QKI expression by targeting the YY1/p65/p300 complex. Overall, our study suggests that the regulatory mechanism of QKI depends on the YY1/p65/p300 complex and that it may serve as a potential target for treatment of HCC. Significance: These findings identify the YY1/p65/p300 complex as a regulator of QKI expression, identifying several potential therapeutic targets for the treatment of HCC.

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“…Regnase-1 reexpression is then ensured by an integrated feedback loop wherein Regnase-1 recognizes and represses its own RNA (Iwasaki et al, 2011). Furthermore, Regnase-1 can be up-regulated by many stimuli, such as IL-17, IL-1β, and TNF signaling (Jeltsch et al, 2014; Garg et al, 2015; Mao et al, 2017; Yang et al, 2018). Overall, Regnase-1 regulation and function have evolved to regulate RNA in the NF-κB pathway in multiple ways.…”

Section: Introductionmentioning

confidence: 99%

Immune homeostasis and regulation of the interferon pathway require myeloid-derived Regnase-3

Gamm

Schaub

Jones

et al. 2019

Journal of Experimental Medicine

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The RNase Regnase-1 is a master RNA regulator in macrophages and T cells that degrades cellular and viral RNA upon NF-κB signaling. The roles of its family members, however, remain largely unknown. Here, we analyzed Regnase-3–deficient mice, which develop hypertrophic lymph nodes. We used various mice with immune cell–specific deletions of Regnase-3 to demonstrate that Regnase-3 acts specifically within myeloid cells. Regnase-3 deficiency systemically increased IFN signaling, which increased the proportion of immature B and innate immune cells, and suppressed follicle and germinal center formation. Expression analysis revealed that Regnase-3 and Regnase-1 share protein degradation pathways. Unlike Regnase-1, Regnase-3 expression is high specifically in macrophages and is transcriptionally controlled by IFN signaling. Although direct targets in macrophages remain unknown, Regnase-3 can bind, degrade, and regulate mRNAs, such as Zc3h12a (Regnase-1), in vitro. These data indicate that Regnase-3, like Regnase-1, is an RNase essential for immune homeostasis but has diverged as key regulator in the IFN pathway in macrophages.

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A super-enhancer maintains homeostatic expression of Regnase-1

Cited by 5 publications

References 23 publications

A Tumor-Specific Super-Enhancer Drives Immune Evasion by Guiding Synchronous Expression of PD-L1 and PD-L2

A Tumor-Specific Super-Enhancer Drives Immune Evasion by Guiding Synchronous Expression of PD-L1 and PD-L2

YY1 Complex Promotes Quaking Expression via Super-Enhancer Binding during EMT of Hepatocellular Carcinoma

Immune homeostasis and regulation of the interferon pathway require myeloid-derived Regnase-3

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