Drug-induced Alterations in the Extracellular Signal-regulated Kinase (ERK) Signalling Pathway: Implications for Reinforcement and Reinstatement

2007 ◽  
Vol 28 (2) ◽  
pp. 157-172 ◽  
Author(s):  
Haifeng Zhai ◽  
Yanqin Li ◽  
Xi Wang ◽  
Lin Lu
Keyword(s):  
Signalling Pathway ◽  
Drug Induced ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal

Regulation of MEK/ERK pathway output by subcellular localization of B-Raf

2012 ◽  
Vol 40 (1) ◽  
pp. 67-72 ◽  
Author(s):  
Catherine Andreadi ◽  
Catherine Noble ◽  
Bipin Patel ◽  
Hong Jin ◽  
Maria M. Aguilar Hernandez ◽  
...  
Keyword(s):  
Growth Factor ◽  
Subcellular Localization ◽  
Signalling Pathway ◽  
Erk Activation ◽  
Extracellular Signal Regulated Kinase ◽  
Intracellular Signalling Pathway ◽  
Pathway Activation ◽  
Extracellular Signal ◽  
A Cell ◽  
Phase Entry

The strength and duration of intracellular signalling pathway activation is a key determinant of the biological outcome of cells in response to extracellular cues. This has been particularly elucidated for the Ras/Raf/MEK [mitogen-activated growth factor/ERK (extracellular-signal-regulated kinase) kinase]/ERK signalling pathway with a number of studies in fibroblasts showing that sustained ERK signalling is a requirement for S-phase entry, whereas transient ERK signalling does not have this capability. A major unanswered question, however, is how a cell can sustain ERK activation, particularly when ERK-specific phosphatases are transcriptionally up-regulated by the pathway itself. A major point of ERK regulation is at the level of Raf, and, to sustain ERK activation in the presence of ERK phosphatases, sustained Raf activation is a requirement. Three Raf proteins exist in mammals, and the activity of all three is induced following growth factor stimulation of cells, but only B-Raf activity is maintained at later time points. This observation points to B-Raf as a regulator of sustained ERK activation. In the present review, we consider evidence for a link between B-Raf and sustained ERK activation, focusing on a potential role for the subcellular localization of B-Raf in this key physiological event.

Xanthohumol inhibits the extracellular signal regulated kinase (ERK) signalling pathway and suppresses cell growth of lung adenocarcinoma cells

Toxicology ◽  
2016 ◽  
Vol 357-358 ◽  
pp. 65-73 ◽  
Author(s):  
Adrianna Sławińska-Brych ◽  
Barbara Zdzisińska ◽  
Magdalena Dmoszyńska-Graniczka ◽  
Witold Jeleniewicz ◽  
Jacek Kurzepa ◽  
...  
Keyword(s):  
Cell Growth ◽  
Lung Adenocarcinoma ◽  
Signalling Pathway ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells

scholarly journals The neuropeptide Galanin is required for homeostatic rebound sleep following increased neuronal activity

2018 ◽  
Author(s):  
Sabine Reichert ◽  
Oriol Pavón Arocas ◽  
Jason Rihel
Keyword(s):  
Neuronal Activity ◽  
Sleep Time ◽  
Drug Induced ◽  
Extracellular Signal Regulated Kinase ◽  
Larval Zebrafish ◽  
Sleep Homeostasis ◽  
Extracellular Signal ◽  
Sleep Homeostat ◽  
Activity Marker ◽  
Molecular Signals

AbstractSleep pressure homeostatically increases during wake and dissipates during sleep, but the molecular signals and neuronal substrates that measure homeostatic sleep pressure remain poorly understood. We present a pharmacological assay in larval zebrafish that generates acute, short-term increases in wakefulness followed by sustained rebound sleep after washout. The intensity of global neuronal activity during drug-induced wakefulness predicted the amount of subsequent rebound sleep. Whole brain mapping with the neuronal activity marker phosphorylated extracellular signal–regulated kinase (pERK) identified preoptic Galanin-expressing neurons as selectively active during rebound sleep, and the relative induction of galanin transcripts was predictive of total rebound sleep time. Galanin is required for sleep homeostasis, as galanin mutants almost completely lacked rebound sleep following both pharmacologically induced neuronal activity and physical sleep deprivation. These results suggest that Galanin plays a key role in responding to sleep pressure signals derived from neuronal activity and functions as an output arm of the vertebrate sleep homeostat. (word count: 158).

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