Key result
TPA induces delayed PGHS-1 synthesis in megakaryocytes through translational cis-element regulation.
Why the study?
The mechanisms underlying the delayed increase in PGHS-1 protein in megakaryocytic cells after TPA treatment were not fully understood, particularly the role of translational regulation.
Population
Megakaryocytic MEG-01 cells
Comparison
TPA-treated cells vs control untreated cells
Design
Preclinical molecular biology study
Follow-up
Up to 4 days
Authors
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Hypothesis-generating for megakaryocyte PGHS-1 control; does not support clinical changes in antiplatelet therapy.
The delayed increase in PGHS-1 protein in megakaryocytic MEG-01 cells following TPA treatment is regulated at the translational level via a specific 45/116-kDa protein complex binding to a conserved 20-nt segment in the 3'-UTR.
Duquette et al. (2002) studied this question. TPA vs. Control cells was evaluated on PGHS-1 protein synthesis and mRNA translation regulation. TPA treatment of megakaryocytic MEG-01 cells induced delayed PGHS-1 protein synthesis at day 4, regulated at the translational level via a 20-nt conserved cis element binding a 45/116-kDa complex.
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