Control mechanisms restricting TF activity in the novel posttranslational role of the poly(adenosine 5′-diphosphate [ADP]-ribose)-polymerase (PARP)-14/tristetraprolin (TTP) pathway. Several mechanisms control TF expression, procoagulant activity, and signaling in various cell types.9 The study of Iqbal et al1 documents a novel posttranscriptional mechanism of TF regulation through selective destabilization of the TF transcript. In this setting, PARP-14 forms ternary complexes containing 3′ AU-rich element (ARE) sequences of the TF mRNA and a regulatory protein, TTP, resulting in accelerated decay of the TF transcript. Obliteration of PARP-14 expression leads to upregulation of TF in macrophages and to exacerbated experimental thrombosis in mice.4 LPA, lipopolysaccharide; PTEN, phosphatase and tensin homolog, tumor suppressor; TFPI, TF pathway inhibitor.

Control mechanisms restricting TF activity in the novel posttranslational role of the poly(adenosine 5′-diphosphate [ADP]-ribose)-polymerase (PARP)-14/tristetraprolin (TTP) pathway. Several mechanisms control TF expression, procoagulant activity, and signaling in various cell types. The study of Iqbal et al documents a novel posttranscriptional mechanism of TF regulation through selective destabilization of the TF transcript. In this setting, PARP-14 forms ternary complexes containing 3′ AU-rich element (ARE) sequences of the TF mRNA and a regulatory protein, TTP, resulting in accelerated decay of the TF transcript. Obliteration of PARP-14 expression leads to upregulation of TF in macrophages and to exacerbated experimental thrombosis in mice. LPA, lipopolysaccharide; PTEN, phosphatase and tensin homolog, tumor suppressor; TFPI, TF pathway inhibitor.

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