Up-regulation of interferon-stimulated gene 15 and its conjugation machinery, UbE1L and UbcH8 expression by tumor necrosis factor-α through p38 MAPK and JNK signaling pathways in human lung carcinoma

Lertsooksawat, Wannee; Wongnoppavich, Ariyaphong; Chairatvit, Kongthawat

doi:10.1007/s11010-019-03609-5

Cited by 14 publications

(17 citation statements)

References 30 publications

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“…ISG15 is a ubiquitin-like protein (Ubl) consisting of two ubiquitinlike domains connected by a short linker (Narasimhan et al, 2005). Expression of ISG15 is induced by type I interferon (IFNa/b) signaling (Farrell et al, 1979), although other innate immune activators can lead to expression of ISG15 (Ashley et al, 2019;Lertsooksawat et al, 2019;Radoshevich et al, 2015). ISG15 was the first Ubl modifier to be described (Haas et al, 1987;Loeb and Haas, 1992), and ISGylation of host and/or pathogen proteins has been best characterized as an antiviral defense mechanism.…”

Section: Introductionmentioning

confidence: 99%

Modulation of Extracellular ISG15 Signaling by Pathogens and Viral Effector Proteins

et al. 2020

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Section: Introductionmentioning

confidence: 99%

Modulation of Extracellular ISG15 Signaling by Pathogens and Viral Effector Proteins

et al. 2020

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“…This also explains the lack of effects on proliferation under high FBS conditions. Interferon-stimulated gene 15 (ISG15) is a member of the ubiquitin-like protein superfamily and induced by type-I IFN (alpha/beta) (Kumar et al, 1993) as well as TNF alpha (Lertsooksawat et al, 2019). ISG15 is conjugated to target proteins by a process called ISGylation to regulate activity of target proteins (Loeb and Haas, 1992).…”

Section: Discussionmentioning

confidence: 99%

RSK1 and RSK2 serine/threonine kinases regulate different transcription programs in cancer

Yang

Caliva²,

Khadka³

et al. 2023

Front. Cell Dev. Biol.

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The 90 kDa ribosomal S6 kinases (RSKs) are serine threonine kinases comprising four isoforms. The isoforms can have overlapping functions in regulation of migration, invasion, proliferation, survival, and transcription in various cancer types. However, isoform specific differences in RSK1 versus RSK2 functions in gene regulation are not yet defined. Here, we delineate ribosomal S6 kinases isoform-specific transcriptional gene regulation by comparing transcription programs in RSK1 and RSK2 knockout cells using microarray analysis. Microarray analysis revealed significantly different mRNA expression patterns between RSK1 knockout and RSK2 knockout cell lines. Importantly some of these functions have not been previously recognized. Our analysis revealed RSK1 has specific roles in cell adhesion, cell cycle regulation and DNA replication and repair pathways, while RSK2 has specific roles in the immune response and interferon signaling pathways. We further validated that the identified gene sets significantly correlated with mRNA datasets from cancer patients. We examined the functional significance of the identified transcriptional programs using cell assays. In alignment with the microarray analysis, we found that RSK1 modulates the mRNA and protein expression of Fibronectin1, affecting cell adhesion and CDK2, affecting S-phase arrest in the cell cycle, and impairing DNA replication and repair. Under similar conditions, RSK2 showed increased ISG15 transcriptional expression, affecting the immune response pathway and cytokine expression. Collectively, our findings revealed the occurrence of RSK1 and RSK2 specific transcriptional regulation, defining separate functions of these closely related isoforms.

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“…Además, se ha observado que en los macró- La proteína ISG15 puede encontrarse en dos estados diferentes: como proteína libre (intracelular o extracelular) o conjugada a proteínas sustrato, tras una modificación postraduccional denominada ISGilación (Figura 7). Tanto ISG15 como las enzimas implicadas en la ISGilación se inducen en respuesta a diferentes IFNs, principalmente de tipo I (a y b) pero también de tipo II (IFNg), y de tipo III (IFNl), así como en respuesta a lipopolisacáridos o TNFa (107,111,(114)(115)(116)(117)(118).…”

Section: Gen Estimulado Por Interferón-15 (Isg15)unclassified

Interferon-stimulated gene 15, a common link of vascular damage in hypertension, obesity and aortic aneurysms

Amor

Redondo

2022

an.ranf

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Hypertension and obesity are major health problems worldwide with significant consequences on morbidity and mortality. In fact, both hypertension and obesity are important risk factors for the development of cardiovascular diseases. Endothelial dysfunction, vascular remodeling, and alterations in vascular mechanics are common aspects of vascular damage in hypertension, obesity, and aneurysms. During the last decades, the importance of low-grade inflammation in vascular damage associated with cardiovascular diseases has been demonstrated. This inflammation is characterized by the accumulation of inflammatory cells in the vasculature, as well as by the increase of local and circulating pro-inflammatory cytokines. Therefore, the identification of new inflammatory mediators involved in this damage has become a very important area of research. Interferón-γ (IFNγ) or tumor necrosis tumoral-α (TNFα) are important cytokines involved in the vascular damage associated with hypertension. Furthermore, it is accepted that TNFα is a key mediator involved in insulin resistance and vascular damage observed in obesity. Both cytokines induce the expression of interferon-stimulated gene 15 (ISG15), a protein similar to ubiquitin that induces a reversible post-translational modification (ISGylation) and that can also be secreted as a free form. The functions of ISG15 are mainly related to the immune response against infections, however, it could also be an interesting new target for cardiovascular damage.

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Up-regulation of interferon-stimulated gene 15 and its conjugation machinery, UbE1L and UbcH8 expression by tumor necrosis factor-α through p38 MAPK and JNK signaling pathways in human lung carcinoma

Cited by 14 publications

References 30 publications

Modulation of Extracellular ISG15 Signaling by Pathogens and Viral Effector Proteins

Modulation of Extracellular ISG15 Signaling by Pathogens and Viral Effector Proteins

RSK1 and RSK2 serine/threonine kinases regulate different transcription programs in cancer

Interferon-stimulated gene 15, a common link of vascular damage in hypertension, obesity and aortic aneurysms

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