Complete abolishment of coagulant activity in monomeric disulfide-deficient tissue factor.
نویسندگان
چکیده
previous PV diagnosis, achieved at least CCyR. In summary, in this larger cohort of CML patients compared with that studied by Makishima et al,1 we found 2.55% of cases presenting concomitant BCR/ABL rearrangement and JAK2V617F mutation, indicating that the simultaneous occurrence of these mutations is rare event but it is not a phoenix; however, while the pathophysiologic significance of this double mutated phenotype remains to be clarified, it seems clear that the predominant clinical phenotype is, in most cases, that of a typical BCR-ABL rearranged CML.
منابع مشابه
Murine tissue factor coagulant activity is critically dependent on the presence of an intact allosteric disulfide.
Tissue factor activation (decryption) has been proposed to be dependent on the cysteine 186-cysteine 209 allosteric disulfide in the tissue factor extracellular domain. Tissue factor procoagulant activity is under the control of protein disulfide isomerase-dependent modulation and nitrosylation of this disulfide. Human tissue factor disulfide mutants have been proposed as a model for encrypted ...
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ورودعنوان ژورنال:
- Blood
دوره 118 12 شماره
صفحات -
تاریخ انتشار 2011