Special Issue "Function and Mechanisms of JNK Pathway"
Deadline for manuscript submissions: closed (30 June 2021) | Viewed by 8080
Interests: JNK in genome expression/gene transcription; JNK in tumorogenesis and regeneration; JNK in metabolism; JNK in immunity; JNK in oxidative stress; JNK in apoptotic cell death mechanisms; JNK in inflammatory processes; JNK in adult brain physiological process; JNK in CNS development (embryonic and postnatal stages); JNK and neuroplasticity; JNK in brain diseases; JNK as a therapeutic target for various biological diseases
JNKs are members of a large group of serine/threonine-directed kinases known as mitogen-activated protein kinases (MAPKs). JNKs are important transducing enzymes that are involved in many biological activities, including cell death and cell survival, inflammatory responses, morphogenesis, cytoskeletal changes, cell proliferation, differentiation, as well as gene expression. Different stress conditions might activate JNK signaling pathway, along with inflammatory signals, growth factors, changes in levels of reactive oxygen species, protein synthesis inhibitors, between other stimuli. In the central nervous system (CNS), JNK activity may be important in developmental stages and in adulthood in situations of absence of stress. Thus in CNS, JNKs are key regulators of brain morphogenesis and developmental death, neuronal migration and pathfinding, axodendritic architecture and synaptic plasticity, with a central role in cognitive function. Different approaches have considered specific proteins of the JNK pathway as a potential therapeutic targets/biomarker to treat human diseases such as diabetes, neurodegenerative conditions, cancer and diseases related with inflammation.
In mammals, there are three genes, namely jnk1 (MAPK8), jnk2 (MAPK9), and jnk3 (MAPK10), that encode for 10 different JNK splice variants. The JNKs activation occurs, after stimulation, through sequentially phosphorylation cascade of three kinases family (MAPK kinase kinase which phosphorylate and activate members of the MAPK kinase family that activate by phosphorylation MAPK proteins). This sequential phosphorylation cascade is facilitated by scaffold JNK-interacting proteins (JIP). The post-translation mechanisms such as acetylation and ubiquitination of members of the MAPK cascade can also affect MAPK activation. The inactivation of this pathway is regulated by MAPK phosphatases (MKPs). More than 50 proteins, located in the cytoplasm and in the nucleus, have been classified as substrates, explaining the elevate range of JNK biological functions.
Dr. Carme Auladell
Dr. Ester Verdaguer
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- c-Jun N-terminal kinase (JNK)
- cell death
- insulin resistance
- brain development
- gene transcription