Control of specificity and magnitude of NF-κB and STAT1-mediated gene activation through PIASy and PIAS1 cooperation

Tahk, Samuel; Liu, Bin; Chernishof, Vasili; Wong, Kelly A.; Wu, Hong; Shuai, Ke

doi:10.1073/pnas.0701877104

Cited by 76 publications

(70 citation statements)

References 21 publications

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“…It has also been shown that genes activated by RelA dimers can be negatively regulated by the E3 ligase PIAS1, a member of the protein inhibitor of activated STAT (PIAS) family [45]. Pias1 −/− mice showed significantly elevated RelA binding to κB sites in genes that also showed hyper-expression [46]. A second line of research provided evidence that promoter-bound RelA and cRel can be phosphorylated by IKK activity thereby catalyzing their degradation [47].…”

Section: Kinetic Control Of the Canonical Pathwaymentioning

confidence: 95%

A single NFκB system for both canonical and non-canonical signaling

et al. 2010

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Two distinct nuclear factor κB (NFκB) signaling pathways have been described; the canonical pathway that mediates inflammatory responses, and the non-canonical pathway that is involved in immune cell differentiation and maturation and secondary lymphoid organogenesis. The former is dependent on the IκB kinase adaptor molecule NEMO, the latter is independent of it. Here, we review the molecular mechanisms of regulation in each signaling axis and attempt to relate the apparent regulatory logic to the physiological function. Further, we review the recent evidence for extensive cross-regulation between these two signaling axes and summarize them in a wiring diagram. These observations suggest that NEMO-dependent and -independent signaling should be viewed within the context of a single NFκB signaling system, which mediates signaling from both inflammatory and organogenic stimuli in an integrated manner. As in other regulatory biological systems, a systems approach including mathematical models that include quantitative and kinetic information will be necessary to characterize the network properties that mediate physiological function, and that may break down to cause or contribute to pathology.

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Section: Kinetic Control Of the Canonical Pathwaymentioning

confidence: 95%

A single NFκB system for both canonical and non-canonical signaling

et al. 2010

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“…PIAS1 and PIASy do not inhibit expression of all ISGs (21,36,37). It is likely that ISGs are divided into distinct groups, partly according to different types of negative regulation under which they are controlled.…”

Section: Discussionmentioning

confidence: 99%

“…LXXLL Motif in the SAP Domain Is Not Involved in the Inhibition of Type I IFN Transcription-PIASy has been reported to inhibit IFN␥-mediated activation of IFN stimulated genes (ISGs) by preventing STAT1-dependent activation of ISRE promoter activity (37,45). Although type I IFN transcription is initially activated by IRF3/7, it is further enhanced by the subsequent IFN-positive feedback loop activated by STAT1 and the ISGF3 complex (46 -48).…”

Section: Piasy Negatively Regulates Virus-induced Type I Ifnmentioning

confidence: 99%

“…In addition, PIAS1 and PIASy regulate LPS-induced cytokine production by inhibiting NFB activity (37,38). Thus, PIAS1 and PIASy play an important role not only in cytokine-mediated JAK/STAT pathways but also in pathogen-activated TLR/RLR pathways of cytokine production (20,39).…”

mentioning

confidence: 99%

“…Among PIAS proteins, PIAS1 and PIASy regulate the specificity and magnitude of cytokine-induced gene expression mediated by STAT1 (36,37). In addition, PIAS1 and PIASy regulate LPS-induced cytokine production by inhibiting NFB activity (37,38).…”

mentioning

confidence: 99%

See 2 more Smart Citations

PIASy Inhibits Virus-induced and Interferon-stimulated Transcription through Distinct Mechanisms

Kubota¹,

Matsuoka

et al. 2011

Journal of Biological Chemistry

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Regulation of early Xenopus development by the PIAS genes

2011

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Originally identified as cytokine inhibitors, protein inhibitors of activated STAT (PIAS) are shown to regulate activities of a plethora of proteins and influence diverse processes such as immune response, cancer formation, and cell cycle progression. However, the roles of PIAS during vertebrate embryogenesis are less understood. In this study, we report isolation and initial characterization of all four PIAS genes from Xenopus laevis. The Xenopus PIAS genes are expressed throughout early development and have overlapping and distinct expression patterns, with for example high levels of PIAS2 in the notochord and strong expression of PIAS4 in the neural and neural crest derivatives. Overexpression of PIAS disrupts mesoderm induction and impairs body axis formation. PIAS proteins have differential ability to regulate signals from the growth factors activin, bone morphogenetic protein 4 (BMP4), and Wnt8. Our data suggest that Xenopus PIAS play important roles in mesodermal induction and patterning during early frog development.

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Control of specificity and magnitude of NF-κB and STAT1-mediated gene activation through PIASy and PIAS1 cooperation

Abstract: NF-B and

Cited by 76 publications

References 21 publications

A single NFκB system for both canonical and non-canonical signaling

A single NFκB system for both canonical and non-canonical signaling

PIASy Inhibits Virus-induced and Interferon-stimulated Transcription through Distinct Mechanisms

Regulation of early Xenopus development by the PIAS genes

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