IndraLab
Statements
reach
"In response to external stimuli, STAT3 is phosphorylated by JAK2 at tyrosine 705 (Tyr705), leading to its translocation from the cytoplasm to the nucleus, which promotes the transcription of various hypertrophic factors, including natriuretic peptide type A (Nppa) and natriuretic peptide type B (Nppb) [18]."
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 ."
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
"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 ]."
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"IL-6 triggers JAK2-dependent phosphorylation of STAT3 Y705, which facilitates STAT3 dimerization and translocation into nucleus to initiate the transcription of a wide spectrum of genes 8. Indeed, knockdown of STAT3 largely abolished Glut5 expression in the IL-6-treated DU145 and HSC-3 cells (Figure 2D)."
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"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
"JAK2 phosphorylates STAT3 at the Y705 residue, which facilitates STAT3 dimerization, nuclear translocation, and activation of its transcriptional activity, thereby promoting the expression of target genes associated with cell proliferation, differentiation, survival, and migration [ xref , xref ]."
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."
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
"In response to external stimuli, STAT3 is phosphorylated by JAK2 at tyrosine 705 (Tyr705), leading to its translocation from the cytoplasm to the nucleus, which promotes the transcription of various hypertrophic factors, including natriuretic peptide type A ( Nppa ) and natriuretic peptide type B ( Nppb ) [ xref ]."
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
"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
"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 participate in the protective effects of vascular endothelial barrier function [35–37]."
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"Therefore, we validated that C21orf58 modulated the cell growth by activating STAT3 signaling.Non‐receptor tyrosine kinase JAK2 phosphorylated the STAT3 at Tyr705 to activate STAT3 activity, then causing STAT3 dimerization and translocation to the nucleus to induce transcription of target genes."
reach
"JAK2 phosphorylates STAT3 at the Y705 residue, which facilitates STAT3 dimerization, nuclear translocation, and activation of its transcriptional activity, thereby promoting the expression of target genes associated with cell proliferation, differentiation, survival, and migration [73, 74]."