C-Jun N-Terminal Kinase
JNK
kinase
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«c-Jun N-terminal kinase (JNKs), were originally identified as kinase that bind and phosphorylate c-Jun on Ser-63 and Ser-73 within its transcriptional activation domain. They belong to the mitogen-activated protein kinase family, and are responsive to stress stimuli, such as cytokines, ultraviolet irradiation, heat shock, and osmotic shock. They also play a role in T cell differentiation and the cellular apoptosis pathway. Activation occurs through a dual phosphorylation of threonine (Thr) and tyrosine (Tyr) residues within a Thr-Pro-Tyr motif located in kinase subdomain VIII. Activation is carried out by two MAP kinase kinase, MKK4 and MKK7, and JNK can be inactivated by Ser/Thr and Tyr protein phosphatases.[1] It has been suggested that this signaling pathway contributes to inflammatory responses in mammals and insects» (wikipedia)
Summary on JNK
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Pathways of JNK
Evidence Sources
Biolinks for JNK are extracted by users from 10 related publications.-
2004Human Cells
- Condition: in in vitro matured human macrophages
- Organism: In vitro
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2004Human Cells
- Organism: In vitro
- Strong Magnitude of Effect.
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2018Human Cells
- Organism: In vitro
- Notable Magnitude of Effect.
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2020Human Cells
- Organism: In vitro
- Notable Magnitude of Effect.
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2020Human Cells
- Organism: In vitro
- Notable Magnitude of Effect.
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2019Human Cells
- Organism: In vitro
- Notable Magnitude of Effect.
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2016Publications Review
- Condition: Obesity
- Organism: Humans
- Strong Magnitude of Effect.
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2020Non-human Cells
- Organism: In vitro
- Notable Magnitude of Effect.
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2021Rodents
- Organism: Mouse / Rat (Rodents)
- Notable Magnitude of Effect.
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2015Rodents
- Organism: Mouse / Rat (Rodents)
- Notable Magnitude of Effect.
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