Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Fatal hemorrhage in mice lacking gamma-glutamyl carboxylase.

Blood - 15 Jun 2007

Zhu Aihua, Sun Hongmin, Raymond Richard M, Furie Barbara C, Furie Bruce, Bronstein Mila, Kaufman Randal J, Westrick Randal, Ginsburg David

Abstract excerpt

The carboxylation of glutamic acid residues to gamma-carboxyglutamic acid (Gla) by the vitamin K-dependent gamma-glutamyl carboxylase (gamma-carboxylase) is an essential posttranslational modification required for the biological activity of a number of proteins, including proteins involved in blood coagulation and its regulation. Heterozygous mice carrying a null mutation at the gamma-carboxylase (Ggcx) gene...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Abdomen
Share to Blood Coagulation Factors
Share to Carbon-Carbon Ligases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Hemorrhage

Share to Mice, Mutant Strains

Share to Phenotype

Share to Survival Rate

Source

Open in PubMed Open full text

Identifiers

PMID: 17327402
DOI: 10.1182/blood-2006-12-064188
PMCID: PMC1890832

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Fatal hemorrhage in mice lacking gamma-glutamyl carboxylase.PMID 17327402Read ↗

Blood coagulation factor X deficiency causes partial embryonic lethality and fatal neonatal bleeding in mice.Semantic proximity Read ↗

γ-Glutamyl carboxylase mutations differentially affect the biological function of vitamin K-dependent proteins.Semantic proximity Read ↗

Vitamin K-dependent coagulation factors deficiency.Semantic proximity Read ↗

Characterization of vitamin K-dependent carboxylase mutations that cause bleeding and nonbleeding disorders.Semantic proximity Read ↗

Vitamin K-dependent gamma-glutamylcarboxylation: an ancient posttranslational modification.Semantic proximity Read ↗

Cellular and biochemical approaches to define GGCX carboxylation of vitamin K-dependent proteins.Semantic proximity Read ↗

Transglutaminases and disease: lessons from genetically engineered mouse models and inherited disorders.Semantic proximity Read ↗

A Missense Mutation in γ-Glutamyl Carboxylase Gene Causes Combined Deficiency of All Vitamin K-Dependent Blood Coagulation FactorsSemantic proximity Read ↗

Targeted inactivation of the mouse locus encoding coagulation factor XIII-A: hemostatic abnormalities in mutant mice and characterization of the coagulation deficit.Semantic proximity Read ↗

Compound heterozygous mutations in the gamma-glutamyl carboxylase gene cause combined deficiency of all vitamin K-dependent blood coagulation factors.Semantic proximity Read ↗

Familial deficiency of vitamin K‐dependent clotting factorsSemantic proximity Read ↗

Mice with a severe deficiency in protein C display prothrombotic and proinflammatory phenotypes and compromised maternal reproductive capabilities.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.