What is the Origin of C-Jun N-Terminal Kinase?

The term is derived from the protein it primarily phosphorylates, the transcription factor c-Jun, and its location of action, the N-terminal region of that protein. Its discovery as a stress-activated protein kinase highlighted a major cellular signaling pathway responsive to environmental insults and internal stressors.

What is the Mechanism of C-Jun N-Terminal Kinase?

JNK acts as a pivotal molecular switch, becoming activated in response to various stressors, including oxidative stress, inflammatory cytokines, and high levels of circulating free fatty acids, a common feature in obesity. Once activated, JNK phosphorylates key substrates, notably the insulin receptor substrate-1 (IRS-1), which subsequently inhibits the downstream signaling cascade of the insulin receptor. This interference effectively blocks insulin's ability to promote glucose uptake, representing a core molecular mechanism linking chronic inflammation and cellular stress to the clinical state of insulin resistance.

C-Jun N-Terminal Kinase

Meaning

C-Jun N-Terminal Kinase, or JNK, is a critical serine/threonine protein kinase belonging to the Mitogen-Activated Protein Kinase (MAPK) family, playing a central role in cellular stress responses. This enzyme is fundamentally involved in regulating cellular proliferation, differentiation, survival, and programmed cell death (apoptosis). In the context of hormonal health, chronic activation of JNK is frequently implicated in the development of insulin resistance and the inflammatory pathways associated with metabolic syndrome.