Evidence map›Paper›PMID 28886871›Full record

ArticleMolecular immunology2018

DAF in diabetic patients is subject to glycation/inactivation at its active site residues.

Rudolf Flückiger, Enzo Cocuzzi, Ram H Nagaraj, Menachem Shoham, Timothy S Kern, M Edward Medof

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. 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

6 authors at 2 institutions in 1 country.

Rudolf FlückigerHarvard Medical School, Boston, MA, USA.
Enzo CocuzziInstitute of Pathology, Case Western Reserve University, Cleveland, OH, USA.
Ram H NagarajDepartment of Ophthalmology, Case Western Reserve University, Cleveland, OH, USA.
Menachem ShohamDepartment of Biochemistry, Case Western Reserve University, Cleveland, OH, USA.
Timothy S KernDepartment of Medicine, Case Western Reserve University, Cleveland, OH, USA; Center for Diabetes Research, Case Western Reserve University, Cleveland, OH, USA.
M Edward MedofInstitute of Pathology, Case Western Reserve University, Cleveland, OH, USA; Department of Ophthalmology, Case Western Reserve University, Cleveland, OH, USA; Department of Medicine, Case Western Reserve University, Cleveland, OH, USA. Electronic address: mxm16@case.edu.
Case Western Reserve University · USHarvard University · US

Funding

TISSUE CULTURE AND HYBRIDOMA MODULEP30EY011373 · NEI · CASE WESTERN RESERVE UNIVERSITY · PI Irina A Pikuleva · 1997 to 2026
$17.7M
Novel therapies to inhibit Diabetic RetinopathyR24EY024864 · NEI · UNIVERSITY OF CALIFORNIA-IRVINE · PI KERN, TIMOTHY S · 2015 to 2019
$8.1M
STUDY OF DIABETIC RETINOPATHYR01EY000300 · NEI · UNIVERSITY OF WISCONSIN MADISON · PI KERN, TIMOTHY S · 1985 to 2013
$4.7M
Role of Photoreceptors in the Pathogenesis of Diabetic RetinopathyR01EY022938 · NEI · UNIVERSITY OF CALIFORNIA-IRVINE · PI KERN, TIMOTHY S · 2013 to 2021
$3.7M
Molecular Mechanisms of Protein Crosslinking in the LensR01EY023286 · NEI · UNIVERSITY OF COLORADO DENVER · PI NAGARAJ, RAM H · 2013 to 2022
$2.9M
Optimizing mesenchymal stem cell and Treg immunosuppression for controlling SLER01AR067182 · NIAMS · CASE WESTERN RESERVE UNIVERSITY · PI MEDOF, MELVIN EDWARD · 2015 to 2019
$1.7M
Local Complement Synthesis and Signaling by Endothelial and Inflammatory CellsR01HL109561 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI MEDOF, MELVIN EDWARD · 2012 to 2015
$1.5M
PROTECTION OF THE OCULAR SURFACER01EY011288 · NEI · CASE WESTERN RESERVE UNIVERSITY · PI MEDOF, MELVIN EDWARD · 1996 to 2006
$1.5M
Acetylation and diabetic retinopathyI01BX002117 · VA · LOUIS STOKES CLEVELAND VA MEDICAL CENTER · PI KERN, TIMOTHY S · 2014 to 2017
–
BLR&D Research Career Scientist ApplicationIK6BX003604 · VA · VETERANS HEALTH ADMINISTRATION · PI KERN, TIMOTHY S · 2017 to 2021
–
BLRD VA I01 BX002117BLRD VA IK6 BX003604NEI NIH HHS P30 EY011373NEI NIH HHS R01 EY000300NEI NIH HHS R01 EY022938NEI NIH HHS R01 EY023286NEI NIH HHS R24 EY024864NHLBI NIH HHS R01 HL109561NIAMS NIH HHS R01 AR067182
6 · The paper itself

Abstract

Decay accelerating factor (DAF or CD55) is a cell associated C3 and C5 convertase regulator originally described in terms of protection of self-cells from systemic complement but now known to modulate adaptive T cell responses. It is expressed on all cell types. We investigated whether nonenzymatic glycation could impair its function and potentially be relevant to complications of diabetes mellitus and other conditions that result in nonenzymatic glycation including cancer, Alzheimer's disease, and aging. Immunoblots of affinity-purified DAF from erythrocytes of patients with diabetes showed pentosidine, glyoxal-AGEs, carboxymethyllysine, and argpyrimidine. HPLC/MS analyses of glucose modified DAF localized the sites of AGE modifications to K

Indexed as

Amino AcidsArginineCatalytic DomainCD55 AntigensComplement ActivationDiabetes MellitusErythrocytesGlucoseGlycation End Products, AdvancedHumansLymphocyte ActivationLysineModels, MolecularOrnithineProtein ConformationPyrimidinesAmino AcidsArginineargpyrimidineCD55 AntigensGlucoseGlycation End Products, AdvancedLysineN(6)-carboxymethyllysineOrnithinepentosidinePyrimidinesRiboseAGEComplementDAFDiabetesGlycation

Identifiers

PMID28886871
PMCPMC5884443
OpenAlexW2752461393

What OpenQuestion holds

Textmetadata
LicenceTDM
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.