Evidence map›Paper›PMID 15039314›Full record

ArticleInfection and immunity2004

N-linked glycosylation is required for c1 inhibitor-mediated protection from endotoxin shock in mice.

Dongxu Liu, Xiaogang Gu, Jennifer Scafidi, Alvin E Davis

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 20% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 39 citations in OpenAlex.

  1. Therapeutic Potential of C1-Inhibitor in Vascular Diseases and Beyond.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Biological activities of C1 inhibitor.Molecular immunology · 2008
    Review
  11. Review
  12. Haploinsufficiency due to deletion within the 3'-UTR of C1-INH-gene associated with hereditary angioedema.Genetics in medicine : official journal of the American College of Medical Genetics · 2006
    Article
  13. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Dongxu LiuCBR Institute for Biomedical Research, Harvard Medical School, Boston, Massachusetts 02115, USA.
Xiaogang Gu
Jennifer Scafidi
Alvin E Davis
Harvard University · US

Funding

C1 INHIBITOR GENE AND HEREDITARY ANGIONEUROTIC EDEMAR37HD022082 · NICHD · IMMUNE DISEASE INSTITUTE, INC. · PI DAVIS, ALVIN E · 1999 to 2008
$3.9M
REGULATION OF C1 INHIBITOR SYNTHESISR01HD033727 · NICHD · IMMUNE DISEASE INSTITUTE, INC. · PI DAVIS, ALVIN E · 1996 to 2004
$1.5M
THE C1 INHIBITOR GENE AND HEREDITARY ANGIONEUROTIC EDEMAR01HD022082 · NICHD · CHILDREN'S HOSPITAL MED CTR (CINCINNATI) · PI DAVIS, ALVIN E · 1987 to 1998
–
NICHD NIH HHS HD22082NICHD NIH HHS HD33727NICHD NIH HHS R01 HD033727NICHD NIH HHS R37 HD022082
6 · The paper itself

Abstract

C1 inhibitor (C1INH) prevents endotoxin shock in mice via a direct interaction with lipopolysaccharide (LPS). This interaction requires the heavily glycosylated amino-terminal domain of C1INH. C1INH in which N-linked carbohydrate was removed by using N-glycosidase F was markedly less effective in protecting mice from LPS-induced lethal septic shock. N-deglycosylated C1INH also failed to suppress fluorescein isothiocyanate (FITC)-LPS binding to and LPS-induced tumor necrosis factor alpha mRNA expression by the murine macrophage-like cell line, RAW 264.7, and cells in human whole blood. In an enzyme linked immunosorbent assay, the N-deglycosylated C1INH bound to LPS very poorly. In addition, C1INH was shown to bind to diphosphoryl lipid A (dLPA) but only weakly to monophosphoryl lipid A (mLPA). As with intact LPS, binding of N-deglycosylated C1INH to dLPA and mLPA was diminished in comparison with the native protein. Removal of O-linked carbohydrate had no effect on any of these activities. Neither detoxified LPS, dLPA, nor mLPA had any effect on the rate or extent of C1INH complex formation with C1s or on cleavage of the reactive center loop by trypsin. These data demonstrate that N-linked glycosylation of C1INH is essential to mediate its interaction with the LPA moiety of LPS and to protect mice from endotoxin shock.

Indexed as

AnimalsCell LineComplement C1 Inactivator ProteinsDisease Models, AnimalEndotoxemiaGlycosylationHumansInflammation MediatorsLeukocytes, MononuclearLipopolysaccharidesMacrophagesMaleMiceMice, Inbred C57BLPeptide-N4-(N-acetyl-beta-glucosaminyl) Asparagine AmidaseComplement C1 Inactivator ProteinsInflammation MediatorsLipopolysaccharidesPeptide-N4-(N-acetyl-beta-glucosaminyl) Asparagine Amidase

Identifiers

PMID15039314
PMCPMC375168
OpenAlexW2143122186

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.