scholarly journals In Murine 3T3 Fibroblasts, Different Second Messenger Pathways Resulting in the Induction of NO Synthase II (iNOS) Converge in the Activation of Transcription Factor NF-B

1996 ◽  
Vol 271 (11) ◽  
pp. 6039-6044 ◽  
Author(s):  
Hartmut Kleinert ◽  
Christian Euchenhofer ◽  
Irmgard Ihrig-Biedert ◽  
Ulrich Förstermann
Keyword(s):  
Transcription Factor ◽  
Second Messenger ◽  
No Synthase ◽  
3T3 Fibroblasts ◽  
Activation Of Transcription ◽  
Second Messenger Pathways

scholarly journals Essential Functions of the Transcription Factor Npas4 in Neural Circuit Development, Plasticity, and Diseases

2020 ◽  
Vol 14 ◽  
Author(s):  
Jian Fu ◽  
Ouyang Guo ◽  
Zhihang Zhen ◽  
Junli Zhen
Keyword(s):  
Transcription Factor ◽  
Neural Circuit ◽  
Second Messenger ◽  
Synaptic Activity ◽  
Postsynaptic Potentials ◽  
Calcium Dependent ◽  
Neural Information ◽  
Formation Function ◽  
Second Messenger Pathways ◽  
Circuit Formation

Signaling from the synapse to nucleus is mediated by the integration and propagation of both membrane potential changes (postsynaptic potentials) and intracellular second messenger cascades. The electrical propagation of postsynaptic potentials allows for rapid neural information processing, while propagating second messenger pathways link synaptic activity to the transcription of genes required for neuronal survival and adaptive changes (plasticity) underlying circuit formation and learning. The propagation of activity-induced calcium signals to the cell nucleus is a major synapse-to-nucleus communication pathway. Neuronal PAS domain protein 4 (Npas4) is a recently discovered calcium-dependent transcription factor that regulates the activation of genes involved in the homeostatic regulation of excitatory–inhibitory balance, which is critical for neural circuit formation, function, and ongoing plasticity, as well as for defense against diseases such as epilepsy. Here, we summarize recent findings on the neuroprotective functions of Npas4 and the potential of Npas4 as a therapeutic target for the treatment of acute and chronic diseases of the central nervous system.

170: Do Alpha1Adrenoceptors in pig Urethra Demonstrate agonist-Specific Coupling to Distinct Second Messenger Pathways ?

2005 ◽  
Vol 173 (4S) ◽  
pp. 46-46
Author(s):  
Rachael L. Scott ◽  
Christopher Chappie ◽  
Russell Chess-Williams
Keyword(s):  
Second Messenger ◽  
Second Messenger Pathways

scholarly journals Suppression of E1A-Mediated Transformation by the p50E4F Transcription Factor

1999 ◽  
Vol 19 (7) ◽  
pp. 4739-4749 ◽  
Author(s):  
Elma R. Fernandes ◽  
Robert J. Rooney
Keyword(s):  
Cell Death ◽  
Transcription Factor ◽  
Suppressive Effect ◽  
Culture Conditions ◽  
Binding Activity ◽  
Cellular Transcription Factor ◽  
Dna Binding Activity ◽  
3T3 Fibroblasts ◽  
Induced Apoptosis ◽  
Nih 3T3

ABSTRACT The adenovirus E1A gene can act as an oncogene or a tumor suppressor, with the latter effect generally arising from the induction of apoptosis or the repression of genes that provide oncogenic growth stimuli (e.g., HER-2/c-erbB2/neu) or increased metastatic invasiveness (e.g., metalloproteases). In this study, coexpression of E1A and p50E4F, a cellular transcription factor whose DNA binding activity is stimulated by E1A, suppressed colony formation by NIH 3T3 cells and transformation of primary rat embryo fibroblasts but had no observed effect in the absence of E1A. Domains in p50E4F required for stimulation of the adenovirus E4 promoter were required for the suppressive effect, indicating a transcriptional mechanism. In serum-containing media, retroviral expression of p50E4F in E1A13S/ras-transformed NIH 3T3 fibroblasts had little effect on subconfluent cultures but accelerated a decline in viability after the cultures reached confluence. Cell death occurred by both apoptosis and necrosis, with the predominance of each process determined by culture conditions. In serum-free media, p50E4F accelerated E1A-induced apoptosis. The results suggest that p50E4F sensitizes cells to signals or conditions that cause cell death.

scholarly journals Repression of ESR1 through Actions of Estrogen Receptor Alpha and Sin3A at the Proximal Promoter

2009 ◽  
Vol 29 (18) ◽  
pp. 4949-4958 ◽  
Author(s):  
Stephanie J. Ellison-Zelski ◽  
Natalia M. Solodin ◽  
Elaine T. Alarid
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Transcription Factor ◽  
Rna Polymerase Ii ◽  
Transcriptional Repression ◽  
Estrogen Receptor Alpha ◽  
Proximal Promoter ◽  
Receptor Alpha ◽  
Expression Of Genes ◽  
Activation Of Transcription

ABSTRACT Gene expression results from the coordinated actions of transcription factor proteins and coregulators. Estrogen receptor alpha (ERα) is a ligand-activated transcription factor that can both activate and repress the expression of genes. Activation of transcription by estrogen-bound ERα has been studied in detail, as has antagonist-induced repression, such as that which occurs by tamoxifen. How estrogen-bound ERα represses gene transcription remains unclear. In this report, we identify a new mechanism of estrogen-induced transcriptional repression by using the ERα gene, ESR1. Upon estrogen treatment, ERα is recruited to two sites on ESR1, one distal (ENH1) and the other at the proximal (A) promoter. Coactivator proteins, namely, p300 and AIB1, are found at both ERα-binding sites. However, recruitment of the Sin3A repressor, loss of RNA polymerase II, and changes in histone modifications occur only at the A promoter. Reduction of Sin3A expression by RNA interference specifically inhibits estrogen-induced repression of ESR1. Furthermore, an estrogen-responsive interaction between Sin3A and ERα is identified. These data support a model of repression wherein actions of ERα and Sin3A at the proximal promoter can overcome activating signals at distal or proximal sites and ultimately decrease gene expression.

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