Figure 2.
Figure 2. Gp130-dependent STAT3 hyperactivation in gp130Y757F/Y757F mice is reduced on a Stat3 heterozygous (Stat3+/-) background. (A) Gp130+/+, gp130Y757F/Y757F, and gp130Y757F/Y757F:Stat3+/- mice were injected with 5 μg IL-6 for the times indicated. Liver lysates were run out on 10% polyacrylamide gel electrophoresis (PAGE) gels, transferred to nitrocellulose membranes, and then immunoblotted with the indicated antibodies. (B) Semiquantitative reverse transcriptase–polymerase chain reaction (RT-PCR) analysis of Socs3 expression was performed on cDNA derived from total RNA prepared from livers of untreated mice. Also shown is the RT-PCR for β-actin as an internal control for sample normalization and integrity.

Gp130-dependent STAT3 hyperactivation in gp130Y757F/Y757F mice is reduced on a Stat3 heterozygous (Stat3+/-) background. (A) Gp130+/+, gp130Y757F/Y757F, and gp130Y757F/Y757F:Stat3+/- mice were injected with 5 μg IL-6 for the times indicated. Liver lysates were run out on 10% polyacrylamide gel electrophoresis (PAGE) gels, transferred to nitrocellulose membranes, and then immunoblotted with the indicated antibodies. (B) Semiquantitative reverse transcriptase–polymerase chain reaction (RT-PCR) analysis of Socs3 expression was performed on cDNA derived from total RNA prepared from livers of untreated mice. Also shown is the RT-PCR for β-actin as an internal control for sample normalization and integrity.

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