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Oncology Glossary

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JAK (Janus kinase): a member of the class of cytoplasmic tyrosine kinases that are involved in signal transduction through a variety of cell-surface receptors, in particular through the family of cytokine receptors. The four mammalian isoforms of JAKs are: JAK1, JAK2, JAK3, and TYK2.

JAK/STAT pathway: the pathway usually (not always) activated by cytokine receptors, where binding of a ligand to the cytokine receptor leads to recruitment and subsequent autophosphorylation of JAK proteins (activated state) at the cellular membrane level. Activated JAKs phosphorylate the receptor, creating docking sites for specific signaling proteins, including STAT proteins. When coupled to the activated receptor, STAT proteins are phosphorylated (activated) by JAK proteins. In contrast to cytokine receptor signaling, receptors with intrinsic tyrosine kinase activity (eg, epidermal growth factor receptor, platelet-derived growth factor) may bypass JAK activation and directly phosphorylate STAT proteins. See JAK (Janus kinase) and STAT.

JCV (JC virus): a human polyomavirus. Infection with JCV and BKV is prevalent in the human population, although the mode of transmission is not clear. BKV and JCV exist as unapparent infections in immunocompetent hosts, but they can produce pathologic effects in immunocompromised individuals through the destruction of infected cells. JCV can cause progressive multifocal leukoencephalopathy, a particular problem for individuals with HIV, and has recently been reported in patients with multiple sclerosis or CrohnÂ’s disease treated with natalizumab.

JNK (Jun kinase): gene that encodes a dual specificity protein kinase that belongs to the Ser/Thr protein kinase family. This kinase is a direct activator of mitogen-activated protein kinases in response to various environmental stresses or mitogenic stimuli. It has been shown to activate MAPK8/JNK1, MAPK9/JNK2, and MAPK14/p38 but not MAPK1/ERK2 or MAPK3/ERK3.

JNK/SAPK: Jun-activated kinase/stress-activated protein kinases, which belong to pathways that are parallel to the mitogenic Raf/MEK/ERK kinase cascade. These kinases are induced in the event of extracellular stresses, including inflammatory cytokines interleukin 1, TNF-α, heat, ultraviolet and ionizing irradiation, and osmotic shock.

Jun: see c-Jun.

JUNB: a member of the early response gene family. The c-Jun (also designated an oncogene) protein product is a key component of the transcriptional factor, AP-1. Along with its normal partner, Fos (a protein product of c-Fos), the Jun-Fos heterodimer acts as a transactivator and plays a key role in regulating gene expression and signal transduction.


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