Defective binding of IRFs to the initiator element of interleukin‐1β‐converting enzyme (ICE) promoter in an interferon‐resistant Daudi subline

Iwase, Satsuki; Furukawa, Yusuke; Kikuchi, Jiro; Saito, Shinobu; Nakamura, Mitsuru; Nakayama, Ritsuko; Horiguchi-Yamada, Junko

doi:10.1016/s0014-5793(99)00515-3

Cited by 13 publications

(20 citation statements)

References 25 publications

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“…Reporter Plasmids and Reporter Assays-The reporter plasmid pC-WT, which contains the human caspase-1 promoter from Ϫ182 to ϩ42 relative to the transcriptional start site cloned upstream of CAT reporter gene has been described (33). The reporter plasmid pC-MTp53, derived from pC-WT by mutating the p53 responsive site, has also been described previously (27).…”

Section: Methodsmentioning

confidence: 99%

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Role of p73 in Regulating Human Caspase-1 Gene Transcription Induced by Interferon-γ and Cisplatin

Jain¹,

Gupta²,

Sudhakar

et al. 2005

Journal of Biological Chemistry

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Section: Methodsmentioning

confidence: 99%

“…Activation of caspase-1 gene expression requires IRF-1 and Stat-1 (24,32). Analysis of the human caspase-1 promoter has shown an IRF-1 binding site, which overlaps with the initiator element (33,34). The IRF-1 binding site is completely conserved in the murine caspase-1 promoter (35).…”

mentioning

confidence: 99%

Role of p73 in Regulating Human Caspase-1 Gene Transcription Induced by Interferon-γ and Cisplatin

Jain¹,

Gupta²,

Sudhakar

et al. 2005

Journal of Biological Chemistry

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“…By computer-assisted promoter analysis of the murine Casp1 and human CASP1 promoters, we identified another potential IRF binding site, designated ISRE II. EMSAs showed enhanced complex formation between ISRE II and nuclear proteins from IRF-2 Ϫ/Ϫ macrophages, despite the fact that ISRE I was originally described as functionally relevant (41). These results could be interpreted as a higher binding of IRF-1 to the promoter sequence as would be expected in the absence of IRF-2.…”

Section: Discussionmentioning

confidence: 80%

“…Although the role of IRFs in the regulation of Casp1 gene expression has been explored previously (32,41), this work sheds new light on the role of IRF-2 in the transcriptional regulation of this gene. Tamura et al (30) first reported that CASP1 gene expression is up-regulated transcriptionally by IRF-1 in T lymphocytes.…”

Section: Discussionmentioning

confidence: 97%

“…Activated macrophages use caspase-1 (also known as IL-1-converting enzyme) to cleave pro-IL-1 and pro-IL-18 to their mature forms, although the role of caspase-1 in the induction of apoptosis seems to be independent of IL-1 or IL-18 secretion (38,39). At least one binding site for IRFs (IFN-stimulated response element (ISRE)) has been identified in the 5Ј flanking region of CASP1 (40), and it has been proposed that Casp1 is regulated transcriptionally by upregulation of IRF-1 and down-regulation of IRF-2 (32,41). Another mechanism that has been reported to cause expression of caspase-1 and apoptosis depends on the activation of STAT1 (13).…”

mentioning

confidence: 99%

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IFN Regulatory Factor-2 Regulates Macrophage Apoptosis through a STAT1/3- and Caspase-1-Dependent Mechanism

Cuesta

Nhu

Zudaire

et al. 2007

The Journal of Immunology

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IFN regulatory factor (IRF)-2 ؊/؊ mice are significantly more resistant to LPS challenge than wild-type littermates, and this was correlated with increased numbers of apoptotic Kupffer cells. To assess the generality of this observation, and to understand the role of IRF-2 in apoptosis, responses of peritoneal macrophages from IRF-2 ؉/؉ and IRF-2 ؊/؊ mice to apoptotic stimuli, including the fungal metabolite, gliotoxin, were compared. IRF-2 ؊/؊ macrophages exhibited a consistently higher incidence of apoptosis that failed to correlate with caspase-3/7 activity. Using microarray gene expression profiling of liver RNA samples derived from IRF-2 ؉/؉ and IRF-2 ؊/؊ mice treated with saline or LPS, we identified >40 genes that were significantly down-regulated in IRF-2 ؊/؊ mice, including Stat3, which has been reported to regulate apoptosis. Compared with IRF-2 ؉/؉ macrophages, STAT3␣ mRNA was up-regulated constitutively or after gliotoxin treatment of IRF-2 ؊/؊ macrophages, whereas STAT3␤ mRNA was down-regulated. Phospho-Y705-STAT3, phospho-S727-STAT1, and phospho-p38 protein levels were also significantly higher in IRF-2 ؊/؊ than control macrophages. Activation of the STAT signaling pathway has been shown to elicit expression of CASP1 and apoptosis. IRF-2 ؊/؊ macrophages exhibited increased basal and gliotoxin-induced caspase-1 mRNA expression and enhanced caspase-1 activity. Pharmacologic inhibition of STAT3 and caspase-1 abolished gliotoxin-induced apoptosis in IRF-2 ؊/؊ macrophages. A novel IFN-stimulated response element, identified within the murine promoter of Casp1, was determined to be functional by EMSA and supershift analysis. Collectively, these data support the hypothesis that IRF-2 acts as a transcriptional repressor of Casp1, and that the absence of IRF-2 renders macrophages more sensitive to apoptotic stimuli in a caspase-1-dependent process.

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POTENTIATION OF FAS- AND TRAIL-MEDIATED APOPTOSIS BY IFN-γ IN A549 LUNG EPITHELIAL CELLS: ENHANCEMENT OF CASPASE-8 EXPRESSION THROUGH IFN-RESPONSE ELEMENT

et al. 2002

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Defective binding of IRFs to the initiator element of interleukin‐1β‐converting enzyme (ICE) promoter in an interferon‐resistant Daudi subline

Cited by 13 publications

References 25 publications

Role of p73 in Regulating Human Caspase-1 Gene Transcription Induced by Interferon-γ and Cisplatin

Role of p73 in Regulating Human Caspase-1 Gene Transcription Induced by Interferon-γ and Cisplatin

IFN Regulatory Factor-2 Regulates Macrophage Apoptosis through a STAT1/3- and Caspase-1-Dependent Mechanism

POTENTIATION OF FAS- AND TRAIL-MEDIATED APOPTOSIS BY IFN-γ IN A549 LUNG EPITHELIAL CELLS: ENHANCEMENT OF CASPASE-8 EXPRESSION THROUGH IFN-RESPONSE ELEMENT

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