Fig. 4.
Fig. 4. The expression of a HIF-1–dependent reporter gene in Hep3B cells transiently cotransfected with plasmids encoding src, a kinase-inactive mutant src or csk. Hep3B cells were cotransfected with the HIF-1 dependent plasmid p(PGK24)3TKGH, the transfection control plasmid pBSα− and either a control plasmid (neo) or plasmids encoding src (src), a kinase-inactive mutant src (src DN), or csk (csk). Twenty-four hours after electroporation, cells were exposed to normoxia (21%) or hypoxia (1%) for 16 hours. Results are expressed as the ratio of reporter growth hormone mRNA to control α-globin mRNA and are the means ± SE of 3 independent experiments. No significant differences in reporter gene expression were seen between control and transfections designed to manipulate src kinase activity.

The expression of a HIF-1–dependent reporter gene in Hep3B cells transiently cotransfected with plasmids encoding src, a kinase-inactive mutant src or csk. Hep3B cells were cotransfected with the HIF-1 dependent plasmid p(PGK24)3TKGH, the transfection control plasmid pBSα and either a control plasmid (neo) or plasmids encoding src (src), a kinase-inactive mutant src (src DN), or csk (csk). Twenty-four hours after electroporation, cells were exposed to normoxia (21%) or hypoxia (1%) for 16 hours. Results are expressed as the ratio of reporter growth hormone mRNA to control α-globin mRNA and are the means ± SE of 3 independent experiments. No significant differences in reporter gene expression were seen between control and transfections designed to manipulate src kinase activity.

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