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STAT5Signal Transducer and Activator of Transcription 5
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Matsumoto A, Masuhara M, Mitsui K, et al CIS, a cytokine inducible SH2 protein, is a target of the JAK-STAT5 pathway and modulates STAT5 activation.
CIS, a cytokine inducible SH2 protein: is a target of the JAK-STAT5 pathway and modulates STAT5 activation.
Although how CALR mutations contribute to the pathogenesis of MPN remain elusive at present, these mutations have been shown to induce the activation of STAT5.
Furthermore, in a recent in vitro study (24), EPO was shown to reduce cisplatin-induced apoptosis in human proximal tubule epithelial cells, while phosphorylation of STAT5 and Akt increased.
They detected EPO throughout the entire process, and their observed results of EPOR, STAT5 and BAX expressions during retinal and lens differentiation suggest that EPOR may play an important part in the normal development of the eye via apoptosis (Wu et al.
Isis also presented new preclinical data showing that the antisense inhibition of STAT5 resulted in potent antitumour activity.
Alteraciones en la activacion de la via JAK2 y STAT5 en higado se han senalado en casos de ayuno (Beauloye, Willems, de Coninck, Frank, Edery, Thissen, 2002) y recientemente lo demostramos en tejido muscular (Calderon, Umana, Sanchez-Gomez, 2004) y linfocitos de bazo (Garzon, 2004) de ratas con restriccion en la proteina dietaria.
Human T-cell leukemia virus type 2 induces survival and proliferation of CD34(+) TF-1 cells through activation of STAT1 and STAT5 by secretion of interferon-gamma and granulocyte macrophage-colony-stimulating factor.
Other signals, including STAT2 (Tyr689), STAT4 (Tyr693), STAT5 (Tyr694), and STAT6 (Tyr641) were all negative during stimulation by IL-27, IFN-a, or IL-17 [Figure 2]c and d.
These disorders appear to be driven, in large part, by the inappropriate activation of growth factor-signaling pathways, and JAK2 is central to signaling from EPOR and TPOR/MPL via STAT5, STAT3, the RAS-MAP kinase pathway, and the PI-3 kinase-AKT pathway.
Flt3/ITD mutation causes constitutive activation of the receptor's tyrosine kinase activity, which results in self activation that stimulates the RAS and STAT5 signal transduction pathways, leading to cell proliferation and progression to AML (11).