Jak-STAT pathway

Jak-STAT pathway

[′jak‚stat ′path‚wā]
(cell and molecular biology)
A rapid signal transduction pathway used by a variety of cytokines and growth factors to alter gene expression. Binding of a cytokine or growth factor to its receptor activates Jak (janus kinase—a cytoplasmic tyrosine kinase) and triggers it to phosphorylate and stimulate STAT (signal transducers and activators of transcription—a gene regulatory protein) to travel to the nucleus and induce transcription of a specific gene.
References in periodicals archive ?
The results could mean "that inhibition of the JAK-STAT pathway may be a new therapeutic target for AD," wrote the study's lead author, Robert Bissonnette, MD, president of Innovaderm Research in Montreal (Br J Dermatol.
Progression of liver disease can be controlled by a number of cellular mediators among which JAK-STAT pathway plays a significant role.
Several of these newly discovered mutations raise the possibility of targeting subpopulations of JMML cases with existing drugs: Janus kinase (JAK) inhibitors, currently used to treat certain other bone marrow and blood cancers such as polycythemia vera, might inhibit signaling through a hyperactive JAK-STAT pathway identified in some patients, while other agents such as 5-azacytidine, most commonly used as a treatment for a blood disorder known as myelodysplastic syndrome, could be used to reduce excessive epigenetic DNA methylation seen in others.
Type Iii interferon (Ifn) induces A Type I IFN-like response in a restricted subset of cells through signaling pathways involving both the Jak-Stat pathway and the mitogen-activated protein kinases.
By targeting the JAK-STAT pathway which is dysregulated in myelofibrosis, Jakavi(R) delivers a rapid and durable benefit that has the potential to make a real difference in the lives of patients with
phagocytophilum at low levels by downregulating some adaptive immune genes and delaying the apoptotic death of neutrophils through activation of the Jak-STAT pathway, among other mechanisms (6), their role as a source of infection for ticks remains to be demonstrated.
Angiotensin II signals mechanical stretch-induced cardiac matrix metalloproteinase expression via JAK-STAT pathway.
Their topics include the role of toll-like receptors in the inmate immune response to RNA viruses, mitochondrial antiviral signaling, the Jak-Stat pathway in response to virus infection, interferons and antiviral action, and human genetic factors involved in viral pathogenesis.
Studies of IFN-induced transcriptional activation uncover the Jak-Stat pathway.