Activation of NF-kappaB, AP-1 and STAT transcription factors is a frequent and early event in human hepatocellular carcinomas

Calcium (Ca2+) signaling in plant cells is an essential and early event during plant-microbe interactions. The recognition of microbe-derived molecules activates Ca2+ channels or Ca2+ pumps that trigger a transient increase in Ca2+ in the cytoplasm. The Ca2+ binding proteins (such as CBL, CPK, CaM, and CML), known as Ca2+ sensors, relay the Ca2+ signal into down-stream signaling events, e.g., activating transcription factors in the nucleus. For example, CaM and CML decode the Ca2+ signals to the CaM/CML-binding protein, especially CaM-binding transcription factors (AtSRs/CAMTAs), to induce the expressions of immune-related genes. In this review, we discuss the recent breakthroughs in down-stream Ca2+ signaling as a dynamic process, subjected to continuous variation and gradual change. AtSR1/CAMTA3 is a CaM-mediated transcription factor that represses plant immunity in non-stressful environments. Stress-triggered Ca2+ spikes impact the Ca2+-CaM-AtSR1 complex to control plant immune response. We also discuss other regulatory mechanisms in which Ca2+ signaling activates CPKs and MAPKs cascades followed by regulating the function of AtSR1 by changing its stability, phosphorylation status, and subcellular localization during plant defense.

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Ozone-induced IL-8 expression and transcription factor binding in respiratory epithelial cells

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.1997.272.3.l504 ◽

1997 ◽

Vol 272 (3) ◽

pp. L504-L511 ◽

Cited By ~ 33

Author(s):

I. Jaspers ◽

E. Flescher ◽

L. C. Chen

Keyword(s):

Transcription Factors ◽

Dna Binding ◽

Epithelial Cells ◽

Inflammatory Cells ◽

Binding Activity ◽

Ozone Exposure ◽

Air Exposure ◽

Dna Binding Activity ◽

Nf Kappab

Ozone, one of the most reactive oxidant gases to which humans are routinely exposed, induces inflammation in the lower airways. The airway epithelium is one of the first targets that inhaled ozone will encounter, but its role in airway inflammation is not well understood. Expression of inducible genes involved in the inflammatory response, such as interleukin (IL)-8, is controlled by transcription factors. Expression of the IL-8 gene is regulated by the transcription factors nuclear factor (NF)-kappaB, NF-IL-6, and possibly activator protein-1 (AP-1). Type II-like epithelial cells (A549) were grown on a collagen-coated membrane and exposed in vitro to 0.1 ppm ozone or air. Exposure to ozone induced DNA-binding activity of NF-kappaB, NF-IL-6, and AP-1. IL-8 mRNA and IL-8 protein levels were also increased after ozone exposure. These results link ozone-induced DNA-binding activity of transcription factors and the production of IL-8 by epithelial cells thus demonstrating a potential cellular cascade resulting in the recruitment of inflammatory cells into the airway lumen.

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SIGNALING INFLAMMATION THROUGH IKK AND THE NF-KAPPAB TRANSCRIPTION FACTORS

Shock ◽

10.1097/00024382-200403001-00175 ◽

2004 ◽

Vol 21 (Supplement) ◽

pp. 44

Author(s):

M Karin ◽

L-W Chen ◽

F. Greten ◽

S. Maeda ◽

J-M Park ◽

...

Keyword(s):

Transcription Factors ◽

Nf Kappab

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Differential expression of the PEA3 subfamily of ETS transcription factors in the mouse ovary and peri-implantation uterus

Reproduction ◽

10.1530/rep.1.00656 ◽

2005 ◽

Vol 129 (5) ◽

pp. 651-657 ◽

Cited By ~ 10

Author(s):

Tae Bon Koo ◽

Haengseok Song ◽

Irene Moon ◽

Kyuyong Han ◽

Chen Chen ◽

...

Keyword(s):

Transcription Factors ◽

Neuronal Development ◽

Early Event ◽

Corpora Lutea ◽

Placental Development ◽

Mouse Ovary ◽

Mouse Uterus ◽

Specific Expression ◽

Low Levels ◽

Spatio Temporal

The objective of the present investigation was to examine the spatio-temporal expression of three members of the ETS family of transcription factors, ERM, ER81, and PEA3, in the peri-implantation mouse uterus and in the ovary. These three factors belong to the PEA3 subfamily and are known to mediate diverse functions ranging from neuronal development to tumor progression. As transcription factors, they regulate the expression of a number of genes with various biological functions. Since several genes with known roles in the reproductive processes have been shown to be under the regulation of one of these factors, we sought to investigate the expression of ERM, ER81, and PEA3 in the mouse ovary and uterus. Quantitative RT-PCR analyses showed that ERM, ER81, and PEA3 were all expressed in the peri-implantation mouse uterus, with higher levels of expression on days 4 and 5 of pregnancy. To determine the cell type-specific expression of these factors, we employedin situhybridization, the results of which revealed that ERM was expressed in both the epithelium and the stroma on days 4 and 5 of pregnancy. Uterine glands showed a high expression of ERM on those days. ERM was also highly expressed in the corpora lutea of the mouse ovary. Both ER81 and PEA3 were expressed at low levels in the stroma on days 4 and 5. On day 8, while ERM and PEA3 were mainly expressed in the embryo and were at low levels in the maternal decidua in a diffused pattern, ER81 was highly expressed in the vascular bed of the mesometrial deciduum. Both ER81 and PEA3 were undetectable in the mouse ovary. Collectively, these data show that ERM is implicated in the early event of implantation as well as in ovarian functions, while ER81 is involved in the establishment of the maternal vasculature for subsequent placental development. PEA3 is apparently an embryonic factor for early embryogenesis.

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The Genomic Response of Tumor Cells to Hypoxia and Reoxygenation. Differential Activation of Transcription Factors AP-1 and NF-kappaB

European Journal of Biochemistry ◽

10.1111/j.1432-1033.1995.632_b.x ◽

1995 ◽

Vol 234 (2) ◽

pp. 632-640 ◽

Cited By ~ 122

Author(s):

Rudolf A. Rupec ◽

Patrick A. Baeuerle

Keyword(s):

Transcription Factors ◽

Tumor Cells ◽

Differential Activation ◽

Activation Of Transcription ◽

Nf Kappab ◽

Genomic Response

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Negative regulation of nuclear factor-kappaB activation and function by glucocorticoids

Journal of Molecular Endocrinology ◽

10.1677/jme.0.0280069 ◽

2002 ◽

Vol 28 (2) ◽

pp. 69-78 ◽

Cited By ~ 157

Author(s):

WY Almawi ◽

OK Melemedjian

Keyword(s):

Transcription Factors ◽

Transcriptional Activation ◽

Promoter Region ◽

Nuclear Translocation ◽

Nuclear Factor Kappab ◽

Nuclear Factor ◽

Creb Binding Protein ◽

Transcriptional Initiation ◽

Nf Kappab ◽

And Function

Glucocorticoids (GCs) exert their anti-inflammatory and antiproliferative effects principally by inhibiting the expression of cytokines and adhesion molecules. Mechanistically, GCs diffuse through the cell membrane, and bind to their inactive cytosolic receptors (GRs), which then undergo conformational modifications that allow for their nuclear translocation. In the nucleus, activated GRs modulate transcriptional events by directly associating with DNA elements, compatible with the GCs response elements (GRE) motif, and located in variable copy numbers and at variable distances from the TATA box, in the promoter region of GC-responsive genes. In addition, activated GRs also acted by antagonizing the activity of transcription factors, in particular nuclear factor-kappaB (NF-kappaB), by direct and indirect mechanisms. GCs induced gene transcription and protein synthesis of the NF-kappaB inhibitor, IkappaB. Activated GR also antagonized NF-kappaB activity through protein-protein interaction involving direct complexing with, and inhibition of, NF-kappaB binding to DNA (Simple Model), or association with NF-kappaB bound to the kappaB DNA site (Composite Model). In addition, and according to the Transmodulation Model, GRE-bound GR may interact with and inhibit the activity of kappaB-bound NF-kappaB via a mechanism involving cross-talk between the two transcription factors. Lastly, GR may compete with NF-kappaB for nuclear coactivators, including CREB binding protein and p300, thereby reducing and inhibiting transcriptional activation by NF-kappaB. It should be noted that, in exerting its effect, activated GR did not affect the correct assembly of the pre-initiation (DAB) complex, but acted rather more proximally in inhibiting the correct assembly of transcription factors in the promoter region, and thus transcriptional initiation.

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p53 regulates epithelial–mesenchymal transition through microRNAs targeting ZEB1 and ZEB2

Journal of Experimental Medicine ◽

10.1084/jem.20110235 ◽

2011 ◽

Vol 208 (5) ◽

pp. 875-883 ◽

Cited By ~ 354

Author(s):

Taewan Kim ◽

Angelo Veronese ◽

Flavia Pichiorri ◽

Tae Jin Lee ◽

Young-Jun Jeon ◽

...

Keyword(s):

Transcription Factors ◽

Tumor Progression ◽

Cell Lines ◽

Epithelial Mesenchymal Transition ◽

Family Members ◽

Mesenchymal Transition ◽

Hepatocellular Carcinomas ◽

Zeb2 Expression

p53 suppresses tumor progression and metastasis. Epithelial–mesenchymal transition (EMT) is a key process in tumor progression and metastasis. The transcription factors ZEB1 and ZEB2 promote EMT. Here, we show that p53 suppresses EMT by repressing expression of ZEB1 and ZEB2. By profiling 92 primary hepatocellular carcinomas (HCCs) and 9 HCC cell lines, we found that p53 up-regulates microRNAs (miRNAs), including miR-200 and miR-192 family members. The miR-200 family members transactivated by p53 then repress ZEB1/2 expression. p53-regulated miR-192 family members also repress ZEB2 expression. Inhibition or overexpression of the miRNAs affects p53-regulated EMT by altering ZEB1 and ZEB2 expression. Our findings indicate that p53 can regulate EMT, and that p53-regulated miRNAs are critical mediators of p53-regulated EMT.

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