MEK/ERK MAP kinase limits poly I:C‐induced antiviral gene expression in RAW264.7 macrophages by reducing interferon‐beta expression

FEBS Letters ◽  
2021 ◽  
Author(s):  
Shawn M. Freed ◽  
Danielle S. Baldi ◽  
Jason A. Snow ◽  
Sierra Athen ◽  
Zachary P. Guinn ◽  
...  
2008 ◽  
Vol 181 (9) ◽  
pp. 6563-6573 ◽  
Author(s):  
Nicola Tamassia ◽  
Vincent Le Moigne ◽  
Marzia Rossato ◽  
Marta Donini ◽  
Stephen McCartney ◽  
...  

Science ◽  
1995 ◽  
Vol 269 (5231) ◽  
pp. 1721-1723 ◽  
Author(s):  
M David ◽  
E Petricoin ◽  
C Benjamin ◽  
R Pine ◽  
M. Weber ◽  
...  

2008 ◽  
Vol 18 (23) ◽  
pp. 1897
Author(s):  
Zoe Hilioti ◽  
Walid Sabbagh ◽  
Saurabh Paliwal ◽  
Adriel Bergmann ◽  
Marcus D. Goncalves ◽  
...  

2021 ◽  
Vol 7 (11) ◽  
pp. eaba1187
Author(s):  
Rina Baba ◽  
Satoru Matsuda ◽  
Yuuichi Arakawa ◽  
Ryuji Yamada ◽  
Noriko Suzuki ◽  
...  

Persistent epigenetic dysregulation may underlie the pathophysiology of neurodevelopmental disorders, such as autism spectrum disorder (ASD). Here, we show that the inhibition of lysine-specific demethylase 1 (LSD1) enzyme activity normalizes aberrant epigenetic control of gene expression in neurodevelopmental disorders. Maternal exposure to valproate or poly I:C caused sustained dysregulation of gene expression in the brain and ASD-like social and cognitive deficits after birth in rodents. Unexpectedly, a specific inhibitor of LSD1 enzyme activity, 5-((1R,2R)-2-((cyclopropylmethyl)amino)cyclopropyl)-N-(tetrahydro-2H-pyran-4-yl)thiophene-3-carboxamide hydrochloride (TAK-418), almost completely normalized the dysregulated gene expression in the brain and ameliorated some ASD-like behaviors in these models. The genes modulated by TAK-418 were almost completely different across the models and their ages. These results suggest that LSD1 enzyme activity may stabilize the aberrant epigenetic machinery in neurodevelopmental disorders, and the inhibition of LSD1 enzyme activity may be the master key to recover gene expression homeostasis. TAK-418 may benefit patients with neurodevelopmental disorders.


2000 ◽  
Vol 292 (4) ◽  
pp. 180-187 ◽  
Author(s):  
R. Pfundt ◽  
M. Wingens ◽  
M. Bergers ◽  
M. Zweers ◽  
M. Frenken ◽  
...  

1995 ◽  
Vol 73 (3-4) ◽  
pp. 133-136 ◽  
Author(s):  
Haleh Vahidi Samiei

Many laboratories, using a variety of organisms, have contributed to deciphering the identity and the order of the components leading from ligand-bound receptor tyrosine kinases to various intracellular events, including changes in gene expression. The gaps have only been filled recently. This minireview summarizes the findings and points out the degree of conservation of the same pathway in distant organisms, both at the molecular level and in terms of the consecutive steps. The review also looks at points at which this pathway might be diverging and points onto which other pathways might be converging. These interactions are not always clear cut, and understanding them will be the challenge for the future.Key words: signal transduction, receptor tyrosine kinase, RAS, RAF, MAP kinase.


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