ArticleBlood2019
A mechanism for hereditary angioedema with normal C1 inhibitor: an inhibitory regulatory role for the factor XII heavy chain.
Article in Blood, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- Clinical features of genetically characterized types of hereditary angioedema with normal C1 inhibitor: a systematic review of qualitative evidence.Orphanet journal of rare diseases · 2020Pooled it
- Cryogenic electron microscopy and coagulation factors.Current opinion in hematology · 2026Review
- Therapeutic Targeting of the Bradykinin B2 Receptor in Immunological and Vascular Diseases: Insights from Kinin Biology to Clinical Outcomes.Clinical reviews in allergy & immunology · 2026Review
- FXII Frameshift Variant Does Not Cause Hereditary Angioedema with Normal C1 Inhibitor.Journal of clinical immunology · 2026Article
- The International/Canadian hereditary angioedema guideline.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2026Review
- Transmission of F12-related hereditary angioedema through a sperm donor.Frontiers in immunology · 2026Article
- Therapeutic Advances in Hereditary Angioedema: A Focus on Present and Future Options.Advances in therapy · 2025Review
- A brief comparison of human factor XII-AlaResearch and practice in thrombosis and haemostasis · 2025Article
- A model of zymogen factor XII: insights into protease activation.Blood advances · 2025Article
- Antithrombotic coating with sheltered positive charges prevents contact activation by controlling factor XII-biointerface binding.Nature materials · 2025Article
- Hereditary Angioedema with Normal C1 Inhibitor: an Updated International Consensus Paper on Diagnosis, Pathophysiology, and Treatment.Clinical reviews in allergy & immunology · 2025Review
- Case Report: Two cases of hereditary angioedema in a Chinese family.Frontiers in allergy · 2025Article
- Evaluating functional C1INH with multiple laboratory methods across Hereditary Angioedema types.Frontiers in immunology · 2025Article
- Factor XII Structure-Function Relationships.Seminars in thrombosis and hemostasis · 2024Review
- A mechanism for hereditary angioedema caused by a methionine-379-to-lysine substitution in kininogens.Blood · 2024Article
- High molecular weight kininogen interactions with the homologs prekallikrein and factor XI: importance to surface-induced coagulation.Journal of thrombosis and haemostasis : JTH · 2024Article
- Circulating prekallikrein levels are correlated with lipid levels in the chinese population: a cross-sectional study.Lipids in health and disease · 2023Article
- A site on factor XII required for productive interactions with polyphosphate.Journal of thrombosis and haemostasis : JTH · 2023Article
- Hereditary angioedema and thrombosis.Blood · 2023Article
- Mechanisms involved in hereditary angioedema with normal C1-inhibitor activity.Frontiers in physiology · 2023Review
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11 authors at 3 institutions in 1 country.
Funding
Abstract
The plasma proteins factor XII (FXII) and prekallikrein (PK) undergo reciprocal activation to the proteases FXIIa and kallikrein by a process that is enhanced by surfaces (contact activation) and regulated by the serpin C1 inhibitor. Kallikrein cleaves high-molecular-weight kininogen (HK), releasing the vasoactive peptide bradykinin. Patients with hereditary angioedema (HAE) experience episodes of soft tissue swelling as a consequence of unregulated kallikrein activity or increased prekallikrein activation. Although most HAE cases are caused by reduced plasma C1-inhibitor activity, HAE has been linked to lysine/arginine substitutions for Thr
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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.