IndraLab
Statements
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"Here, we demonstrated that despite the propensity to produce more IL-6 from APC ( xref ), IL-6 induced STAT3 phosphorylation in neonatal T FH cells was reduced compared to those of adult cells, a likely consequence of the reduced expression of the GP130 component of IL-6R complex on neonatal T FH cells."
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"Because IL-6 has been found to increase the levels of serine pSTAT3 and induce the phosphorylation of STAT3 on tyrosine residues XREF_BIBR, we incubated CLL cells with 30 mg/ml rhIL-6 for 20 minutes and analyzed their miR-155 expression levels at different times following incubation using RT-PCR and relative qRT-PCR."
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"In brain cortex, increased UA : (1) reduced tMCAO induced increases in Vegfa and Mmp9 and Timp1 ratio expressions; (2) induced Sod2 and Cat expressions and reduced MDA levels; (3) induced Il6 expression, upregulated STAT3 and NF-kappaB p65 phosphorylation, induced Socs3 expression, and inhibited microglia activation; and (4) ameliorated the Bax and Bcl -2 ratio and induced a reduction in caspase-3 cleavage as well as in TUNEL positive cell counts."
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"IL-6 increased phosphorylation of STAT3 (at Tyr (705)) and ERK1/2 (at Tyr (204)) within 5 min that peaked at 15-30 min and returned to basal levels at 2 h. Phosphorylation of STAT3 was blocked by genistein, a protein tyrosine kinase inhibitor, and AG490, a JAK2 inhibitor, but not PD98059, an ERK1/2 kinase inhibitor."