Calcium-mediated Gene Expression: Mechanism for Neuronal Plasticity and Survival

1995 ◽  
Vol 1 (6) ◽  
pp. 317-320 ◽  
Author(s):  
Steven Finkbeiner
Keyword(s):  
Gene Expression ◽  
Neuronal Plasticity ◽  
Expression Mechanism

Plant microRNAs: master regulator of gene expression mechanism

2015 ◽  
Vol 39 (11) ◽  
pp. 1185-1190 ◽  
Author(s):  
Riddhi Datta ◽  
Soumitra Paul
Keyword(s):  
Gene Expression ◽  
Master Regulator ◽  
Expression Mechanism

A priori, de novo mathematical exploration of gene expression mechanism via regression viewpoint with briefly cataloged modeling antiquity

2016 ◽  
Vol 10 (01) ◽  
pp. 1750006
Author(s):  
Shaurya Jauhari ◽  
S. A. M. Rizvi
Keyword(s):  
Gene Expression ◽  
De Novo ◽  
A Priori ◽  
Mathematical Framework ◽  
Reaction Synthesis ◽  
Expression Data ◽  
Boolean Models ◽  
Mathematical Exploration ◽  
Mathematical Techniques ◽  
Expression Mechanism

Various algorithms have been devised to mathematically model the dynamic mechanism of the gene expression data. Gillespie’s stochastic simulation (GSSA) has been exceptionally primal for chemical reaction synthesis with future ameliorations. Several other mathematical techniques such as differential equations, thermodynamic models and Boolean models have been implemented to optimally and effectively represent the gene functioning. We present a novel mathematical framework of gene expression, undertaking the mathematical modeling of the transcription and translation phases, which is a detour from conventional modeling approaches. These subprocesses are inherent to every gene expression, which is implicitly an experimental outcome. As we foresee, there can be modeled a generality about some basal translation or transcription values that correspond to a particular assay.

scholarly journals Noradrenergic Modulation of Light-Driven Egr-1 Expression in the Adult Visual Cortex

2011 ◽  
Vol 5 ◽  
pp. JEN.S6497 ◽  
Author(s):  
Liisa A. Tremere
Keyword(s):  
Gene Expression ◽  
Visual Cortex ◽  
Neuronal Plasticity ◽  
Adrenergic Receptor ◽  
Receptor Activation ◽  
Early Gene ◽  
Receptor Subtype ◽  
Vertebrate Species ◽  
Regulated Gene Expression ◽  
Noradrenergic Modulation

Noradrenaline has been shown to modulate sensory driven responses in the primary visual cortex (V1) of a number of vertebrate species. Moreover, this neurotransmitter has been postulated to bridge neuronal activation to genomic responses in order to instruct cells in long-lasting changes in neuronal performance. Here we show that local noradrenergic receptor activation in V1 is required for experience-regulated gene expression in the mouse V1. More specifically, we demonstrate that noradrenaline used locally within V1 mediates the light-driven gene expression of egr-1, an immediate early gene implicated as a mediator of neuronal plasticity. Visually-driven egr-1 expression largely depends on the α-adrenergic receptor subtype, with a lesser involvement of the β-subtype. Our findings suggest that noradrenergic transmission regulates plasticity associated gene expression in V1 of awake mice and is well positioned to broadly integrate experience-dependent changes at the cell's membrane and the genomic machinery in neurons.

scholarly journals Tat has a dual role in simian immunodeficiency virus transcription

2012 ◽  
Vol 93 (10) ◽  
pp. 2279-2289 ◽  
Author(s):  
Gisela J. van der Velden ◽  
Monique A. Vink ◽  
Ben Berkhout ◽  
Atze T. Das
Keyword(s):  
Gene Expression ◽  
Simian Immunodeficiency Virus ◽  
Cultured Cells ◽  
Virus Transcription ◽  
Immunodeficiency Virus ◽  
Dna Elements ◽  
Tar Rna ◽  
Essential Function ◽  
Expression Mechanism

Tat has a pivotal role in human and simian immunodeficiency virus (HIV and SIV) replication because it stimulates transcription by binding to the trans-activator response (TAR) element. In addition, several other Tat functions have been proposed. Most studies have focused on HIV-1 Tat and much less is known about SIV Tat. An SIVmac239 variant was constructed previously in which the Tat–TAR transcription mechanism is functionally replaced by the doxycycline-inducible Tet-On gene expression mechanism (SIV-rtTA). In this study, SIV-rtTA variants were used to analyse the functions of SIV Tat. It was shown that Tat-minus SIV-rtTA variants replicated efficiently in PM1 T-cells, ruling out an additional essential Tat function. Nevertheless, replication was suboptimal in other cells, and evolutionary pressure to repair Tat expression was documented. It was demonstrated that SIV-rtTA required Tat for optimal gene expression, despite the absence of the Tat–TAR axis. This Tat effect was lost upon replacement of the long terminal repeat promoter region by a non-related promoter. These results indicate that Tat can activate SIV transcription via TAR RNA and U3 DNA elements but has no other essential function in replication in cultured cells. The experiments were limited to cell lines and PBMCs, and did not exclude an accessory Tat function under specific conditions or in vivo.

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