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After treatment with CoCl, BPC157-treated HUVECs failed to form tube-like structures (Supplementary Figure S3B), which is consistent with our analysis that the redox state is a key determinant of BACH1s functional direction

View Study [2]"Extracellular signal-regulated kinase and phosphoinositol-3 kinase mediate IGF-1 induced proliferation of fetal cardiomyocytes" Sundgren NC, Giraud GD, et al., 2003 Finding: Researchers found that Long R3 IGF-I stimulates cell proliferation (hyperplasia) through both ERK and PI3K signaling pathwaysthis explains the unique ability of IGF-1 to create new cells, not just make existing cells bigger

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