Corrigendum for Zhuang D et al., Volume 286/55, June 2004, p. H2103–H2112

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Abstract
[ ARTICLE][1] Pages H2103–H2112 : Zhuang D, Ceacareanu A-C, Lin Y, Ceacareanu B, Dixit M, Chapman KE, Waters CM, Rao GN, and Hassid A. “Nitric oxide attenuates insulin- or IGF-I-stimulated aortic smooth muscle cell motility by decreasing H2O2 levels: essential role of cGMP”. Figure 8 B should appear as follows: ![Fig. 8.][2] Fig. 8. NO donor, cGMP, or catalase block IGF-I-induced tyrosine phosphorylation of IGF-I receptor (IGF-IR). Cells were pretreated with 30 μM DETANO for 30 min, 30 μM 8-p-CPT-cGMP for 10 min, or 0.3 μM catalase for 180 min, followed by treatment with 3.3 nM IGF-I for 5 min. IGF-IR was then immunoprecipitated and the levels of phosphotyrosine and IGF-IR were determined by sequential Western blot analyses. A : the top blot shows phosphotyrosine levels in receptor protein, whereas the bottom blot shows IGF-I receptor protein levels, via reprobe of the blot shown at top . B : quantitative summary of four Western blot experiments. Results are given as the ratio of phosphotyrosine to IGF-IR levels (means ± SE). * P < 0.05 compared with control. [1]: /lookup/volpage/286/H2103 [2]: pending:yes

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