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, 154 (3), 665-70

Pathways of Egr-1-mediated Gene Transcription in Vascular Biology


Pathways of Egr-1-mediated Gene Transcription in Vascular Biology

E S Silverman et al. Am J Pathol.


Figure 1.
Figure 1.
Model of injury-induced PDGF A-chain gene transcription. Endothelial injury releases FGF-2, which binds to its tyrosine kinase receptor and activates ERK and JNK kinases in a paracrine fashion. These kinases phosphorylate ternary complex factors (TCF), which cooperate with serum response factor (SRF) to induce Egr-1 transcription. Egr-1 can displace Sp1 and other transcription factors from the G+C-rich region of target genes and increase transcription above basal levels through multiple protein-protein interactions with CBP/p300. The basal transcription apparatus (B) is indicated. The number of interactions is related to the number and position of Egr-1 consensus binding sites within the promoter. Other transcription factors (?) may be involved. Activated genes may alter cell growth, migration, adhesion, and survival. For example, the released PDGF A-chain binds to receptors on local cells, stimulating growth and migration of adjacent vascular smooth muscle cells.

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