Evidences p(HGNC:PIN1) to p(HGNC:SMAD2)

The high degree of colocalization between pSmad2/3 and ubiquitin (Figure 7) provides additional evidence for a forced degradation of Smad2 via the proteasome pathway in AD which is controlled through binding of Pin1

Alltogether, this provides evidence for a negative feed-back regulation of Pin1 by Smad. A similar mechanism might be instrumental in AD, where nuclear Smad concentrations are significantly reduced , which potentially contributes to increased levels of Pin1 [16]

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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.