ArticleResearch and practice in thrombosis and haemostasis2018
Protein S K196E mutation reduces its cofactor activity for APC but not for TFPI.
Article in Research and practice in thrombosis and haemostasis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 8 citations in OpenAlex.
- [From structure to function: new developments in the interaction of coagulation factor Ⅴ with tissue factor pathway inhibitor α].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2026Review
- Protein S: a vitamin K-dependent factor bridging haemostasis, tissue homeostasis and cancer.The Biochemical journal · 2026Review
- Novel monoclonal antibodies for an activated protein C cleavage neoepitope of coagulation factor Va.Research and practice in thrombosis and haemostasis · 2026Article
- Carrier frequencies of antithrombin, protein C, and protein S deficiency variants estimated using a public database and expression experiments.Research and practice in thrombosis and haemostasis · 2021Article
- Protein S K196E mutation reduces its cofactor activity for APC but not for TFPI.Research and practice in thrombosis and haemostasis · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundProtein S (PS) is an anticoagulant molecule that functions as a cofactor for activated protein C (APC) in the inactivation of activated coagulation factors Va (FVa) and VIIIa. It also serves as a cofactor for tissue factor pathway inhibitor (TFPI) in the efficient inhibition of factor Xa (FXa). The Lys
objectivesTo investigate the molecular basis of the thrombophilic phenotype of Japanese patients carrying the PS K196E mutation.
methodsWe expressed recombinant human PS wild-type (PS-K) and K196E-mutant (PS-E) in CHO cells, and purified them by Ni
resultsPS-E had approximately 40% APC cofactor activity compared with PS-K in a clotting-based assay and a FVa inactivation assay. The TFPI cofactor activity of PS-E in the FXa inactivation assay was equivalent to that of PS-K in the absence and presence of coagulation factor V. The strengths of PS-E and PS-K binding to the β chain of C4BP were comparable, and both were equally cleaved by thrombin.
conclusionsThe PS K196E mutation increases the risk of VTE because of reduced APC cofactor activity but does not alter various other properties, including the TFPI cofactor activity.
Indexed as
Identifiers
What OpenQuestion holds
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.