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

Protein C mutation (A267T) results in ER retention and unfolded protein response activation.

PloS one - 1 Jan 2011

Tjeldhorn Lena, Iversen Nina, Sandvig Kirsten, Bergan Jonas, Sandset Per Morten, Skretting Grethe

Abstract excerpt

BACKGROUND: Protein C (PC) deficiency is associated with a high risk of venous thrombosis. Recently, we identified the PC-A267T mutation in a patient with PC deficiency and revealed by in vitro studies decreased intracellular and secreted levels of the mutant. The aim of the present study was to characterize the underlying mechanism(s). METHODOLOGY/PRINCIPAL FINDINGS: CHO-K1 cells stably expressing the wild-type...

Read the complete abstract on PubMed

Topics

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

Share to Endoplasmic Reticulum Stress
Share to Apoptosis

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Blotting, Western

Share to CHO Cells

Share to Cricetinae

Share to Endoplasmic Reticulum

Share to Protein C

Share to Unfolded Protein Response

Source

Open in PubMed Open full text

Identifiers

PMID: 21901152
DOI: 10.1371/journal.pone.0024009
PMCID: PMC3162024

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Protein C mutation (A267T) results in ER retention and unfolded protein response activation.PMID 21901152Read ↗

Functional characterization of the protein C A267T mutation: evidence for impaired secretion due to defective intracellular transport.Semantic proximity Read ↗

Functional characterization of two protein C variants causing type I deficiency via cellular degradation or retention.Semantic proximity Read ↗

Homozygous protein C deficiency with late onset venous thrombosis: identification and in vitro expression study of a novel Pro275Ser mutation.Semantic proximity Read ↗

Proteasome degradation of protein C and plasmin inhibitor mutants.Semantic proximity Read ↗

Defective sorting to secretory vesicles in trans-Golgi network is partly responsible for protein C deficiency: molecular mechanisms of impaired secretion of abnormal protein C R169W, R352W, and G376D.Semantic proximity Read ↗

Molecular characterization of p.Asp77Gly and the novel p.Ala163Val and p.Ala163Glu mutations causing protein C deficiency.Semantic proximity Read ↗

Molecular basis of inherited protein C deficiency results from genetic variations in the signal peptide and propeptide regions.Semantic proximity Read ↗

The protein C pathwaysSemantic proximity Read ↗

Two novel compound heterozygous mutations associated with types I and II protein C deficiency with unusual phenotypes.Semantic proximity Read ↗

Factor VIII exhibits chaperone-dependent and glucose-regulated reversible amyloid formation in the endoplasmic reticulumSemantic proximity Read ↗

Protein C.Semantic proximity Read ↗

Activation of Endoplasmic Reticulum Stress and Unfolded Protein Response in Congenital Factor VII Deficiency.Semantic proximity Read ↗

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