IndraLab
Statements
sparser
"Furthermore, treatment of JAK2 clinical medicine AZD1480 to ESCC cells showed similar tendency with Lico B. Thus, JAK2 downstream signaling proteins phosphorylation of STAT3 at Y705 and S727 as well as STAT3 target protein Mcl-1 expression was decreased with treatment of Lico B. Our results suggest that Lico B inhibits ESCC cell growth, arrests cell cycle and induces apoptosis, revealing the underlying mechanism involved in JAK2/STAT3 signaling pathways after Lico B treatment."
sparser
"Also, JAK2 phosphorylates STAT3 at Tyr705, inducing its dimerization and translocation to the nucleus where it regulates the expression of different proteins involved in cancer progression, such as cyclin D1, COX2, VEGF, and SOCS3, a negative regulator of leptin signaling [ xref , xref ]."
sparser
"As JAK2 directly phosphorylates STAT3 at Tyr705, we next examined the possible interactions of DLEC1 with STAT3 and JAK2 by reciprocal co-immunoprecipitation (co-IP) experiments with Flag or DLEC1, STAT3 and JAK2 antibodies in carcinoma (KYSE150, H1299) and immortalized cells (HEK293T)."
reach
"As JAK2 directly phosphorylates STAT3 at Tyr705, we next examined the possible interactions of DLEC1 with STAT3 and JAK2 by reciprocal co-immunoprecipitation (co-IP) experiments with Flag or DLEC1, STAT3 and JAK2 antibodies in carcinoma (KYSE150, H1299) and immortalized cells (HEK293T)."
sparser
"Finally, the JAK2 kinase may induce phosphorylation of Tyr705 on the STAT3 that bound with the receptor, and then the activated STAT3 would enter the nucleus in a form of a dimer to bind specifically with the DNA sequences to trigger the expression of downstream target genes such as cyclin D1 , c-myc , c-Jun , bcl , bcl-xL , and mcl-I . These genes were reported to modulate the cell cycle and inhibit the cell apoptosis, which may be participated in the protective effects of vascular endothelial barrier function [ xref – xref ]."
sparser
"JAK2 phosphorylates STAT3 on its Y705 residue, resulting in the dimerization and nuclear translocation of STAT3 and activation of STAT3 transcriptional activity, leading to the expression of STAT3 target genes that promote cell proliferation, differentiation, survival, and migration [ xref , xref , xref ]."
"Inactive cytoplasmic STATs are recruited to the activated receptor by docking of the STAT SH2 domain to selected receptor tyrosine phosphopeptides, where they are in turn phosphorylated on a single tyrosine by Jak kinases. Has been identified tyrosine 705 of Stat3 as the likely site of phosphorylation by Jak kinases during signal transduction."
reach
"In bone metastatic prostate cancer, IHC analyses have identified that the majority of cases studied are positive for STAT3, and kinome profiling have shown elevated activity of JAK2, which phosphorylates STAT3 at Tyr705 resulting in head to tail dimerization, translocation to the nucleus and binding to the promoters of target survival genes such as BCL-xL and survivin 59."
rlimsp
"Furthermore, the phosphorylation at Tyr705 of STAT3, which is known to be a phosphorylation site for Janus kinase 2 (JAK2), was completely inhibited by purvalanol A early (3 h) after drug treatment, although the phosphorylation of STAT3 at Ser727, which is a phosphorylation site for Ras/Raf/MEK and extracellular signal-regulated protein kinase 1/2, was still detectable until late (12 h) after treatment."
sparser
"In bone metastatic prostate cancer, IHC analyses have identified that the majority of cases studied are positive for STAT3, and kinome profiling have shown elevated activity of JAK2, which phosphorylates STAT3 at Tyr705 resulting in head to tail dimerization, translocation to the nucleus and binding to the promoters of target survival genes such as BCL-xL and survivin xref ."
reach
"The proximity of JAK2 and STAT3 promotes the phosphorylation of STAT3 at tyrosine-705 (Y705) initiating the translocation of STAT3 to the nucleus, where it functions as a transcription factor, initiating the gene expression of the genes involved in tumourigenesis (Figure 2) [38,39]."
sparser
"Finally, the JAK2 kinase may induce phosphorylation of Tyr705 on the STAT3 that bound with the receptor, and then the activated STAT3 would enter the nucleus in a form of a dimer to bind specifically with the DNA sequences to trigger the expression of downstream target genes such as cyclin D1, c-myc, c-Jun, bcl, bcl-xL, and mcl-I. These genes were reported to modulate the cell cycle and inhibit the cell apoptosis, which may participate in the protective effects of vascular endothelial barrier function [35–37]."