ReviewCurrent opinion in hematology2017
Single-chain factor XII: a new form of activated factor XII.
Review in Current opinion in hematology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- A phase I, first-in-human, randomized dose-escalation study of anti-activated factor XII monoclonal antibody garadacimab.Clinical and translational science · 2022Trial
- Revisiting the Link Between Factor XII and Recurrent Pregnancy Loss: A Scoping Review.American journal of reproductive immunology (New York, N.Y. : 1989) · 2025Article
- Crystal structure of coagulation factor XII N-terminal domains 1-5.Acta crystallographica. Section D, Structural biology · 2025Article
- Targeting the Contact Pathway of Coagulation for the Prevention and Management of Medical Device-Associated Thrombosis.Seminars in thrombosis and hemostasis · 2024Review
- Model for surface-dependent factor XII activation: the roles of factor XII heavy chain domains.Blood advances · 2022Article
- Proteolytic activity of contact factor zymogens.Journal of thrombosis and haemostasis : JTH · 2021Review
- Protease activity in single-chain prekallikrein.Blood · 2020Article
- Antibody inhibition of contact factor XII reduces platelet deposition in a model of extracorporeal membrane oxygenator perfusion in nonhuman primates.Research and practice in thrombosis and haemostasis · 2020Article
- A non-circulating pool of factor XI associated with glycosaminoglycans in mice.Journal of thrombosis and haemostasis : JTH · 2019Article
- Article
- Factor XII-Driven Inflammatory Reactions with Implications for Anaphylaxis.Frontiers in immunology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
Abstract
purpose of reviewExposure of blood to foreign surfaces induces reciprocal conversion of the plasma proteins factor XII (fXII) and plasma prekallikrein (PPK) to the proteases α-fXIIa and α-kallikrein. This process, called contact activation, has a range of effects on host defence mechanisms, including promoting coagulation. The nature of the triggering mechanism for contact activation is debated. One hypothesis predicts that fXII has protease activity, either intrinsically or upon surface-binding, that initiates contact activation. We tested this by assessing the proteolytic activity of a recombinant fXII variant that cannot be converted to α-fXIIa. RECENT
findingsThe proteolytic activity of fXII-T (for 'triple' mutant), a variant with alanine substitutions for arginine at activation cleavage sites (Arg334, Arg344, and Arg353) was tested with known α-fXIIa substrates. FXII-T activates PPK in solution, and the reaction is enhanced by polyphosphate, an inducer of contact activation released from platelets. In the presence of polyphosphate, fXII-T converts fXII to α-fXIIa, and also converts the coagulation protein factor XI to its active form. SUMMARY: The findings support the hypothesis that contact activation is initiated through activity intrinsic to single-chain fXII, and indicate that preexisting α-fXIIa is not required for induction of contact activation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.