IndraLab

Statements


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"Lastly, pretreatment of cells with ruxolitinib for two hours abrogated the interferon response of ACE2 and STAT1 (Fig. 6c)."

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"At 24 hours, compared with untreated cells, there was some persistent elevation of phospho-STAT1, which ruxolitinib and fedratinib reduced."

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"Ruxolitinib only partially attenuated IFN-α induced loss of quiescence in Jak2 LT-HSCs (Fig. 7e), again demonstrating that LT-HSC pSTAT1 signaling was unable to be completely blocked by ruxolitinib."

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"Ruxolitinib inhibits IFN-gamma-induced pro-inflammatory effects by targeting the JAK/STAT1 axis."

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"Inhibition of STAT1 by Ruxolitinib Abolishes Induction of PDL-1 on Monocytes by Paracrine Factors ."

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"As shown in XREF_FIG, ruxolitinib decreased JAK1, JAK2, STAT1 and pSTAT1 (S727) protein levels in a dose dependent manner in LS411N and SW620 cells."

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"Ruxolitinib treatment significantly reduced tumor volume, STAT1 activation, and oncogenic transcriptional factors ETV1/4/5."
| PMC

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"It has been revealed that Ruxolitinib, a Jak/STAT inhibitor, promotes CTL infiltration in the tumor microenvironment in the pancreatic cancer mice model by selectively inhibiting STAT1 and STAT3 activation."

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"To date, myelofibrosis treatment of two patients with Ruxolitinib, which inhibits JAK1,2 and likely STAT1, is hypothesized to have contributed to the development of cryptococcosis in these individuals [27, 28]."

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"As expected, treatment with Ruxolitinib was sufficient to completely inhibit IFNγ-induced upregulation of Stat1 and Gbp2 in MLL-AF9 transformed FLCs (Supplementary Fig. 6E)."

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"Mechanistically , ruxolitinib inhibited the secretion of IL-6 , TNF and MCP1 and the expression of STAT1 but promoted the expression of STAT6 in macrophages in vitro , indicating that M1 macrophage polarization to M2 occurred through activation of the STAT6-IRF4 pathway ."

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"At 4 hours, compared with TNF-α alone, treatment with either 0.4 μM ruxolitinib or 1 μM fedratinib significantly reduced STAT1 (Figure 1B) and STAT3 signaling (Figure 1C) at similar levels."

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"In all used iMGL lines, control and SPG11, ruxolitinib pretreatment significantly reduced STAT1 and CXCL10 signal intensity after IFNγ stimulation (Fig. 6a, b; Online Resource Fig. 7e)."

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"In these experiments, we confirmed that SB431542 and ruxolitinib suppressed pSMAD2 and pSTAT1 in hCECs by western blotting, and cell death in hCECs was largely not induced at the concentrations used in this experiment by TUNEL assay (Supplementary Fig. S5, S6)."

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"Interestingly ex vivo treatment with ruxolitinib was able to completely block STAT1, suggesting an inadequate intracellular drug concentration in LT-HSCs [172]."

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"Finally, Ruxolitinib administration can limit STAT1 activation in patients carrying STAT1 gain of function mutations."

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"Tofacitinib and ruxolitinib suppress STAT1 activation in TNF-stimulated RA synovial macrophages (41)."

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"Ruxolitinib may be predicted to block STAT1 activation through inhibition of JAK1."

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"Ruxolitinib additionally decreased activation of STAT1 in immune effector cells."

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"This mechanism may be relevant in CML, since it was shown that cells of IFNa-resistant patients lack STAT1 expression [17] and in PV, when STAT1 function is inhibited by ruxolitinib."

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"Surprisingly, Ruxolitinib treatment decreased pSTAT1 at every time point (Fig 5C)."

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"Since Ruxolitinib inhibits pSTAT1 by negatively regulating JAK activity by competitive inhibition at the active sites, and not by dephosphorylation or by deactivating JAK1/2, the JAK/STAT1 signaling pathway may still be engaged despite being actively inhibited."

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"In accordance with our findings in the aGVHD murine model, ruxolitinib inhibited activation of the JAK2/STAT1 pathway in aGVHD patient–derived BMSCs (Figure 9H)."

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"In addition, treatment of mice with the JAK/STAT pathway inhibitor ruxolitinib during the onset of brain inflammation led to reductions in JAK/STAT transcriptional targets in brains as well as p-STAT1/STAT3 on western blots, brain edema, and brain-infiltrating T cells and monocytes, but clinical improvement was complicated by increases in brain fungal loads."

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"1muM of Ruxolitinib (JAK1/2 inhibitor) and 5muM of Tofacitinib (JAK1/3 inhibitor) suppressed the IL-27-mediated STAT-1, -3 and -5 activation (XREF_SUPPLEMENTARY) without any significant change in cell viability (data not shown)."

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"Addition of ruxolitinib and baricitinib inhibited STAT1 hyperactivation in STAT1-GoF EPSC in a dose-dependent manner, which was not observed with tofacitinib."

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"Furthermore, we established that specific STAT1 inhibition by ruxolitinib (Ruxo) reduces M-like macrophage activation in Tfr2 macrophages."

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"Ruxolitinib, a JAK1/2 inhibitor, suppressed STAT1 activation (online supplemental figure S4)."

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"Ruxolitinib suppresses the hyperresponsiveness of STAT1 to ligand stimulation, leading to the normalization of Th1 and follicular T helper cell responses (112), and the partial rescue of NK cell differentiation and function (109)."

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"JAK-STAT inhibitor Ruxolitinib selectively inhibits STAT1 and STAT3 activation and increases CTL infiltration to induce a Tc1 and Th1 immune response in the tumor microenvironment in an orthotopic pancreatic cancer mouse model."

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"There was an over 20-fold difference in the potency of ruxolitinib inhibition of STAT1 and STAT3 phosphorylation (IC 50 of 1.3 x10 -8 M), as compared with STAT5 phosphorylation (IC 50 of 2.8 x10 -7 M) (XREF_FIG)."

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"With regard to endogenous IFNs, treatment of HIEs with ruxolitinib to block STAT1 activation and inhibit ISG induction facilitates replication of HAstV1, VA1, and MLB1 as well as a clinical HAstV isolate, though notably with differences in response across distinct HIE lines, indicating variation among donor genotypes in HAstV-mediated IFN regulation ( Figure 2C ) (73)."