ArticleOncotarget2016
A plasma proteolysis pathway comprising blood coagulation proteases.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Comparative analysis of obesity-related cardiometabolic and renal biomarkers in human plasma and serum.Scientific reports · 2019Trial
- Targeted dual degradation of HER2 and EGFR obliterates oncogenic signaling, overcomes therapy resistance, and inhibits metastatic lesions in HER2-positive breast cancer models.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2024Article
- Blood Coagulation and Beyond: Position Paper from the Fourth Maastricht Consensus Conference on Thrombosis.Thrombosis and haemostasis · 2023Article
- Anti-HK antibody inhibits the plasma contact system by blocking prekallikrein and factor XI activation in vivo.Blood advances · 2023Article
- Depleting receptor tyrosine kinases EGFR and HER2 overcomes resistance to EGFR inhibitors in colorectal cancer.Journal of experimental & clinical cancer research : CR · 2022Article
- Anti-HK antibody reveals critical roles of a 20-residue HK region for Aβ-induced plasma contact system activation.Blood advances · 2022Article
- Insight into the human pathodegradome of the V8 protease from Staphylococcus aureus.Cell reports · 2021Article
- The root cause of drug resistance in HER2-positive breast cancer and the therapeutic approaches to overcoming the resistance.Pharmacology & therapeutics · 2021Review
- Complement Activation in the Central Nervous System: A Biophysical Model for Immune Dysregulation in the Disease State.Frontiers in molecular neuroscience · 2021Article
- Current Understanding of the Emerging Role of Prolidase in Cellular Metabolism.International journal of molecular sciences · 2020Review
- Ulceration in Prolidase Deficiency: Successful Treatment with Anticoagulants.Acta dermato-venereologica · 2020Article
- Factor VII Gene Defects: Review of Functional Studies and Their Clinical ImplicationsIranian biomedical journal · 2019Review
- A recombinant human protein targeting HER2 overcomes drug resistance in HER2-positive breast cancer.Science translational medicine · 2019Article
- Blood will out: vascular contributions to Alzheimer's disease.The Journal of clinical investigation · 2018Review
- Anticoagulants inhibit proteolytic clearance of plasma amyloid beta.Oncotarget · 2018Article
- PEPD is a pivotal regulator of p53 tumor suppressor.Nature communications · 2017Article
- Interactions of β-amyloid peptide with fibrinogen and coagulation factor XII may contribute to Alzheimer's disease.Current opinion in hematology · 2017Review
- Dual inhibition of ErbB1 and ErbB2 in cancer by recombinant human prolidase mutant hPEPD-G278D.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Coagulation factors are essential for hemostasis. Here, we show that these factors also team up to degrade plasma proteins that are unrelated to hemostasis. Prolidase, SRC and amyloid β1-42 (Aβ1-42) are used as probes. Each probe, upon entering the blood circulation, binds and activates factor XII (FXII), triggering the intrinsic and common coagulation cascades, which in turn activate factor VII, a component of the extrinsic coagulation cascade. Activated factor VII (FVIIa) rapidly degrades the circulating probes. Therefore, FXII and FVIIa serve as the sensor/initiator and executioner, respectively, for the proteolysis pathway. Moreover, activation of this pathway by one probe leads to the degradation of all three probes. Significant activation of this pathway follows tissue injury and may also occur in other disorders, e.g., Alzheimer's disease, of which Aβ1-42 is a key driver. However, enoxaparin, a clinically used anticoagulant, inhibits the proteolysis pathway and elevates plasma levels of the probes. Enoxaparin may also mitigate potential impact of activators of the proteolysis pathway on coagulation. Our results suggest that the proteolysis pathway is important for maintaining low levels of various plasma proteins. Our finding that enoxaparin inhibits this pathway provides a means to control it. Inhibition of this pathway may facilitate the development of disease biomarkers and protein therapeutics, e.g., plasma Aβ1-42 as a biomarker of Alzheimer's disease or recombinant human prolidase as an antitumor agent.
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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.