scholarly journals Critical Role of the Automodification of Poly(ADP-ribose) Polymerase-1 in Nuclear Factor-κB-dependent Gene Expression in Primary Cultured Mouse Glial Cells

2004 ◽  
Vol 279 (41) ◽  
pp. 42774-42786 ◽  
Author(s):  
Hidemitsu Nakajima ◽  
Hiroshi Nagaso ◽  
Nobukazu Kakui ◽  
Midori Ishikawa ◽  
Toyokazu Hiranuma ◽  
...  
Keyword(s):  
Gene Expression ◽  
Glial Cells ◽  
Critical Role ◽  
Nuclear Factor Κb ◽  
Nuclear Factor

scholarly journals Essential Role of Transcription Factor Nuclear Factor-κB in Regulation of Interleukin-8 Gene Expression by Nitrite Reductase from Pseudomonas aeruginosa in Respiratory Epithelial Cells

1999 ◽  
Vol 67 (8) ◽  
pp. 3872-3878 ◽  
Author(s):  
Naoki Mori ◽  
Kazunori Oishi ◽  
Borann Sar ◽  
Naofumi Mukaida ◽  
Tsuyoshi Nagatake ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pseudomonas Aeruginosa ◽  
Epithelial Cells ◽  
Nitrite Reductase ◽  
Critical Role ◽  
Nuclear Factor Κb ◽  
Interleukin 8 ◽  
Nuclear Factor ◽  
Respiratory Cells

ABSTRACT Persistent infection with Pseudomonas aeruginosaincreases interleukin-8 (IL-8) levels and causes dense neutrophil infiltrations in the airways of patients with chronic airway diseases. Recently, we have reported that nitrite reductase from P. aeruginosa induces the production of IL-8 in respiratory cells, including bronchial epithelial cells. To determine the molecular mechanism(s) of nitrite reductase-induced IL-8 expression in respiratory cells, A549 epithelial cells were transfected with plasmids containing serial deletions of the 5′-flanking region of the IL-8 gene and then exposed to nitrite reductase. Nitrite reductase significantly enhanced IL-8 gene promoter-driven reporter activity. This increased IL-8 gene expression was inhibited by mutating the nuclear factor-κB (NF-κB) binding element. Nitrite reductase enhanced nuclear localization of the NF-κB binding complex. Furthermore, nitrite reductase induced the degradation of IκBα, the major cytoplasmic inhibitor of NF-κB, and the expression of IκBα mRNA. These data support the critical role of the activation of NF-κB in nitrite reductase-induced IL-8 gene expression in airway epithelium.

scholarly journals Role of Nuclear Factor-κB in the Antiviral Action of Interferon and Interferon-regulated Gene Expression

2004 ◽  
Vol 279 (30) ◽  
pp. 31304-31311 ◽  
Author(s):  
Lawrence M. Pfeffer ◽  
Jong-Gwan Kim ◽  
Susan R. Pfeffer ◽  
Dennis J. Carrigan ◽  
Darren P. Baker ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Antiviral Action ◽  
Regulated Gene Expression

Critical role of nuclear factor‐κB and stress‐activated protein kinases in steroid unresponsiveness

2002 ◽  
Vol 16 (13) ◽  
pp. 1-19 ◽  
Author(s):  
Heike Bantel ◽  
M. Lienhard Schmitz ◽  
Armin Raible ◽  
Michael Gregor ◽  
Klaus Schulze‐Osthoff
Keyword(s):  
Protein Kinases ◽  
Critical Role ◽  
Nuclear Factor Κb ◽  
Nuclear Factor

Regulation of cyclin D1 gene expression

2010 ◽  
Vol 38 (1) ◽  
pp. 217-222 ◽  
Author(s):  
Ini-Isabée Witzel ◽  
Li Fang Koh ◽  
Neil D. Perkins
Keyword(s):  
Gene Expression ◽  
Cyclin D1 ◽  
Rna Processing ◽  
Dominant Role ◽  
Rna Stability ◽  
Transcriptional Regulator ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Post Transcriptional Regulation

Cyclin D1 is a key regulator of cell proliferation and its expression is subject to both transcriptional and post-transcriptional regulation. In different cellular contexts, different pathways assume a dominant role in regulating its expression, whereas their disregulation can contribute to overexpression of cyclin D1 in tumorigenesis. Here, we discuss the ability of the NF-κB (nuclear factor κB)/IKK [IκB (inhibitor of NF-κB) kinase] pathways to regulate cyclin D1 gene transcription and also consider the newly discovered role of the SNARP (SNIP1/SkIP-associated RNA processing) complex as a co-transcriptional regulator of cyclin D1 RNA stability.

scholarly journals A critical role of TAK1 in B-cell receptor–mediated nuclear factor κB activation

Blood ◽  
2009 ◽  
Vol 113 (19) ◽  
pp. 4566-4574 ◽  
Author(s):  
James Schuman ◽  
Yuhong Chen ◽  
Andrew Podd ◽  
Mei Yu ◽  
Hong-Hsing Liu ◽  
...  
Keyword(s):  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Critical Role ◽  
Cell Receptor ◽  
Nuclear Factor Κb ◽  
Cell Development ◽  
B Cell Receptor ◽  
Nuclear Factor

Abstract The kinase TAK1 is essential for T-cell receptor (TCR)–mediated nuclear factor κB (NF-κB) activation and T-cell development. However, the role of TAK1 in B-cell receptor (BCR)–mediated NF-κB activation and B-cell development is not clear. Here we show that B-cell–specific deletion of TAK1 impaired the transition from transitional type 2 to mature follicular (FO) B cells and caused a marked decrease of marginal zone (MZ) B cells. TAK1-deficient B cells exhibited an increase of BCR-induced apoptosis and impaired proliferation in response to BCR ligation. Importantly, TAK1-deficient B cells failed to activate NF-κB after BCR stimulation. Thus, TAK1 is critical for B-cell maturation and BCR-induced NF-κB activation.

scholarly journals Anacardic acid (6-nonadecyl salicylic acid), an inhibitor of histone acetyltransferase, suppresses expression of nuclear factor-κB–regulated gene products involved in cell survival, proliferation, invasion, and inflammation through inhibition of the inhibitory subunit of nuclear factor-κBα kinase, leading to potentiation of apoptosis

Blood ◽  
2008 ◽  
Vol 111 (10) ◽  
pp. 4880-4891 ◽  
Author(s):  
Bokyung Sung ◽  
Manoj K. Pandey ◽  
Kwang Seok Ahn ◽  
Tingfang Yi ◽  
Madan M. Chaturvedi ◽  
...  
Keyword(s):  
Salicylic Acid ◽  
Histone Acetyltransferase ◽  
Critical Role ◽  
Nuclear Factor Κb ◽  
Chemotherapeutic Agents ◽  
Anacardic Acid ◽  
Nuclear Factor ◽  
Gene Products ◽  
Down Regulation

Abstract Anacardic acid (6-pentadecylsalicylic acid) is derived from traditional medicinal plants, such as cashew nuts, and has been linked to anticancer, anti-inflammatory, and radiosensitization activities through a mechanism that is not yet fully understood. Because of the role of nuclear factor-κB (NF-κB) activation in these cellular responses, we postulated that anacardic acid might interfere with this pathway. We found that this salicylic acid potentiated the apoptosis induced by cytokine and chemotherapeutic agents, which correlated with the down-regulation of various gene products that mediate proliferation (cyclin D1 and cyclooxygenase-2), survival (Bcl-2, Bcl-xL, cFLIP, cIAP-1, and survivin), invasion (matrix metalloproteinase-9 and intercellular adhesion molecule-1), and angiogenesis (vascular endothelial growth factor), all known to be regulated by the NF-κB. We found that anacardic acid inhibited both inducible and constitutive NF-κB activation; suppressed the activation of IκBα kinase that led to abrogation of phosphorylation and degradation of IκBα; inhibited acetylation and nuclear translocation of p65; and suppressed NF-κB–dependent reporter gene expression. Down-regulation of the p300 histone acetyltransferase gene by RNA interference abrogated the effect of anacardic acid on NF-κB suppression, suggesting the critical role of this enzyme. Overall, our results demonstrate a novel role for anacardic acid in potentially preventing or treating cancer through modulation of NF-κB signaling pathway.

scholarly journals Cyclooxygenase-2 Regulated by the Nuclear Factor-κB Pathway Plays an Important Role in Endometrial Breakdown in a Female Mouse Menstrual-like Model

Endocrinology ◽  
2013 ◽  
Vol 154 (8) ◽  
pp. 2900-2911 ◽  
Author(s):  
Xiangbo Xu ◽  
Xihua Chen ◽  
Yunfeng Li ◽  
Huizi Cao ◽  
Cuige Shi ◽  
...  
Keyword(s):  
Critical Role ◽  
Nuclear Factor Κb ◽  
Pcr Analysis ◽  
Pyrrolidine Dithiocarbamate ◽  
Nuclear Factor ◽  
Cox Inhibitor ◽  
Cox 2

Abstract The role of prostaglandins (PGs) in menstruation has long been proposed. Although evidence from studies on human and nonhuman primates supports the involvement of PGs in menstruation, whether PGs play an obligatory role in the process remains unclear. Although cyclooxygenase (COX) inhibitors have been used in the treatment of irregular uterine bleeding, the mechanism involved has not been elucidated. In this study, we used a recently established mouse menstrual-like model for investigating the role of COX in endometrial breakdown and its regulation. Administration of the nonspecific COX inhibitor indomethacin and the COX-2 selective inhibitor DuP-697 led to inhibition of the menstrual-like process. Furthermore, immunostaining analysis showed that the nuclear factor (NF)κB proteins P50, P65, and COX-2 colocalized in the outer decidual stroma at 12 to 16 hours after progesterone withdrawal. Chromatin immunoprecipitation analysis showed that NFκB binding to the Cox-2 promoter increased at 12 hours after progesterone withdrawal in vivo, and real-time PCR analysis showed that the NFκB inhibitors pyrrolidine dithiocarbamate and MG-132 inhibited Cox-2 mRNA expression in vivo and in vitro, respectively. Furthermore, COX-2 and NFκB inhibitors similarly reduced endometrial breakdown, suggesting that NFκB/COX-2-derived PGs play a critical role in this process. In addition, the CD45+ leukocyte numbers were sharply reduced following indomethacin (COX-1 and COX-2 inhibitor), DuP-697 (COX-2 inhibitor), and pyrrolidine dithiocarbamate (NFκB inhibitor) treatment. Collectively, these data indicate that NFκB/COX-2-induced PGs regulate leukocyte influx, leading to endometrial breakdown.

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