| General information | Literature | Expression | Regulation | Mutation | Interaction |
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Basic Information |
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|---|---|
Gene ID | 8682 |
Name | PEA15 |
Synonymous | HMAT1|HUMMAT1H|MAT1|MAT1H|PEA-15|PED;phosphoprotein enriched in astrocytes 15;PEA15;phosphoprotein enriched in astrocytes 15 |
Definition | 15 kDa phosphoprotein enriched in astrocytes|astrocytic phosphoprotein PEA-15|homolog of mouse MAT-1 oncogene|mammary transforming gene 1, mouse, homolog of|phosphoprotein enriched in diabetes |
Position | 1q21.1 |
Gene type | protein-coding |
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Title |
Abstract |
| Phosphorylation is the switch that turns PEA-15 from tumor suppressor to tumor promoter. | Abnormal ERK signaling is implicated in many human diseases including cancer. This signaling cascade is a good target for the therapy of certain malignancies because of its important role in regulating cell proliferation and survival. The small phosphoprotein PEA-15 is a potent regulator of the ERK signaling cascade, and, by acting on this pathway, has been described to have both tumor-suppressor and tumor-promoter functions. However, the exact mechanism by which PEA-15 drives the outcome one way or the other remains unclear. We propose that the cellular environment is crucial in determining PEA-15 protein function by affecting the proteins phosphorylation state. We hypothesize that only unphosphorylated PEA-15 can act as a tumor-suppressor and that phosphorylation alters the interaction with binding partners to promote tumor development. In order to use PEA-15 as a prognostic marker or therapeutic target it is therefore important to evaluate its phosphorylation status. |