Journal
BLOOD
Volume 100, Issue 1, Pages 359-362Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2002-02-0412
Keywords
-
Categories
Funding
- NHLBI NIH HHS [K08 HL03661] Funding Source: Medline
- NIDDK NIH HHS [P30 DK50306] Funding Source: Medline
Ask authors/readers for more resources
The activated form of prothrombin plays pivotal roles in the regulation of crucial coagulation, fibrinolytic, and cellular processes. Among several congenital genetic defects affecting the prothrombin gene, a G-->A mutation at position 20210-the accepted polyadenylation site-has been linked to hyperprothrombinemia and a corresponding increase in venous and arterial thrombotic risk. The current study substantiates the hypothesis that the 20210A mutation effects posttranscriptional dysregulation of the prothrombin messenger RNA (mRNA). Moreover, data from experiments carried out in fresh liver tissue indicate that the 20210A mutation does not affect prothrombin mRNA stability but, rather, effects a change in the location of the 3'-cleavage/polyadenylation reaction. Based upon this evidence, we propose an alternate model for the dysregulated expression of the prothrombin 20210A gene that does not require a change in the stability of its mRNA.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available