General characteristics of JNK activation pathways.
DOI:
https://doi.org/10.11603/mcch.2410-681X.2016.v0.i4.7289Keywords:
c-Jun N-terminal proteinkinase, mitogen-activated proteinkinase, reactive oxygen species, stress EPR, fatty acids, methylglyoxal, sphingolipids.Abstract
c-Jun N-terminal protein kinase (JNK) – members of motogen-activated proteinkinase (MAP-kinases) families a activate in response to various factors, oxidative, thermal, osmotic stress, the effect on the cells of cytokines and growth factors, and many others are among them. Their activation is involved in the pathogenesis of insulin resistance, diabetes and related pathologies. This fact is determined the choice of JNK, as a therapeutic target for new drugs design.
The aim of this work was the analysis and synthesis of information on the ways of JNK activation, as well as the basic cell metabolites that are also involved in this process.
There are basic pathways of JNK activation, including MAP kinase cascade start mediated interaction of ligands with receptors on the plasma membrane, reactive oxygen species formation, and endoplasmic reticulum stress. The main cellular metabolites involved in activation of JNK are methylglyoxal, lyso- and sphingolipids, fatty acids (FFA).
In the cell at the same time, there are several major enzyme activation mechanisms. Some metabolites, particularly FFA and lysolipids have their own activation pathways. There is tissue specificity of JNK activation, it is important to consider in the design of new JNK inhibitors.
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