Evidence map›Paper›PMID 28364129›Full record

ArticleImmunogenetics2017

The scavenging capacity of DMBT1 is impaired by germline deletions.

Floris J Bikker, Caroline End, Antoon J M Ligtenberg, Stephanie Blaich, Stefan Lyer, Marcus Renner, Rainer Wittig, Kamran Nazmi, Arie van Nieuw Amerongen, Annemarie Poustka and 2 more

Abstract read
In one paragraph

Article in Immunogenetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

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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

12 authors.

Floris J BikkerDepartment of Oral Biochemistry, Academic Centre for Dentistry Amsterdam, University of Amsterdam and VU University Amsterdam, Gustav Mahlerlaan 3004, 1081LA, Amsterdam, Netherlands. fbikker@acta.nl.
Caroline EndDivision of Molecular Genome Analysis, German Cancer Research Center, Heidelberg, Germany.
Antoon J M LigtenbergDepartment of Oral Biochemistry, Academic Centre for Dentistry Amsterdam, University of Amsterdam and VU University Amsterdam, Gustav Mahlerlaan 3004, 1081LA, Amsterdam, Netherlands.
Stephanie BlaichDivision of Molecular Genome Analysis, German Cancer Research Center, Heidelberg, Germany.
Stefan LyerDivision of Molecular Genome Analysis, German Cancer Research Center, Heidelberg, Germany.
Marcus RennerDivision of Molecular Genome Analysis, German Cancer Research Center, Heidelberg, Germany.
Rainer WittigDivision of Molecular Genome Analysis, German Cancer Research Center, Heidelberg, Germany.
Kamran NazmiDepartment of Oral Biochemistry, Academic Centre for Dentistry Amsterdam, University of Amsterdam and VU University Amsterdam, Gustav Mahlerlaan 3004, 1081LA, Amsterdam, Netherlands.
Arie van Nieuw AmerongenDepartment of Oral Biochemistry, Academic Centre for Dentistry Amsterdam, University of Amsterdam and VU University Amsterdam, Gustav Mahlerlaan 3004, 1081LA, Amsterdam, Netherlands.
Annemarie PoustkaDivision of Molecular Genome Analysis, German Cancer Research Center, Heidelberg, Germany.
Enno C I VeermanDepartment of Oral Biochemistry, Academic Centre for Dentistry Amsterdam, University of Amsterdam and VU University Amsterdam, Gustav Mahlerlaan 3004, 1081LA, Amsterdam, Netherlands.
Jan MollenhauerDivision of Molecular Genome Analysis, German Cancer Research Center, Heidelberg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Scavenger Receptor Cysteine-Rich (SRCR) proteins are an archaic group of proteins characterized by the presence of multiple SRCR domains. They are membrane-bound or secreted proteins, which are generally related to host defense systems in animals. Deleted in Malignant Brain Tumors 1 (DMBT1) is a SRCR protein which is secreted in mucosal fluids and involved in host defense by pathogen binding by its SRCR domains. Genetic polymorphism within DMBT1 leads to DMBT1-alleles giving rise to polypeptides with interindividually different numbers of SRCR domains, ranging from 8 SRCR domains (encoded by 6 kb DMBT1 variant) to 13 SRCR domains (encoded by the 8 kb DMBT1 variant). In the present study, we have investigated whether reduction from 13 to 8 amino-terminal SRCR domains leads to reduction of bacterial binding. The 6 kb variant bound ~20-45% less bacteria compared to the 8 kb variant. These results support the hypothesis that genetic variation in DMBT1 may influence microbial defense.

Indexed as

Germ-Line MutationSequence DeletionBacterial AdhesionCalcium-Binding ProteinsDNA-Binding ProteinsHumansPolymorphism, GeneticProtein BindingProtein Interaction Domains and MotifsReceptors, Cell SurfaceReceptors, ScavengerTumor Suppressor ProteinsCalcium-Binding ProteinsDMBT1 protein, humanDNA-Binding ProteinsReceptors, Cell SurfaceReceptors, ScavengerTumor Suppressor ProteinsGenetic polymorphismMicrobial defensePathogen bindingSRCR domain

Identifiers

PMID28364129
PMCPMC5435793

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Registered trials

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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.