Fig. 5.
Fig. 5. (A) Src kinase activity in fibroblasts derived from mice deficient in src (src−) or csk (csk−). The results are expressed as the ratio of activity to that wild-type fibroblast cells (src wt) and are the means ± SE of 6 independent experiments. As would be anticipated, the cells deficient in src had negligible src kinase activity, while those deficient in the regulatory csk had significantly increased activity. (*P < .05). (B) RNase protection analysis of gene expression. The cells were exposed in parallel to varying oxygen concentrations for 4 hours (21%, 1%, 0.1%, and anoxia). Results are expressed as the ratio of the mRNA of interest to that of the actin control (×100) and are the means ± SE of 5 independent experiments. Despite the substantial differences in src kinase activity between the cells, no significant differences were seen in the expression of VEGF or Glut-1 at any oxygen tension.

(A) Src kinase activity in fibroblasts derived from mice deficient in src (src) or csk (csk). The results are expressed as the ratio of activity to that wild-type fibroblast cells (src wt) and are the means ± SE of 6 independent experiments. As would be anticipated, the cells deficient in src had negligible src kinase activity, while those deficient in the regulatory csk had significantly increased activity. (*P < .05). (B) RNase protection analysis of gene expression. The cells were exposed in parallel to varying oxygen concentrations for 4 hours (21%, 1%, 0.1%, and anoxia). Results are expressed as the ratio of the mRNA of interest to that of the actin control (×100) and are the means ± SE of 5 independent experiments. Despite the substantial differences in src kinase activity between the cells, no significant differences were seen in the expression of VEGF or Glut-1 at any oxygen tension.

Close Modal

or Create an Account

Close Modal
Close Modal