Evidence map›Paper›PMID 32545641›Full record

ArticleInternational journal of molecular sciences2020

Molecular Interactions Stabilizing the Promatrix Metalloprotease-9·Serglycin Heteromer.

Rangita Dawadi, Nabin Malla, Beate Hegge, Imin Wushur, Eli Berg, Gunbjørg Svineng, Ingebrigt Sylte, Jan-Olof Winberg

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2020. 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
–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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
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

8 authors.

Rangita DawadiDepartment of Medical Biology, Faculty of Health Sciences, UiT-The Arctic University of Norway, 9037 Tromsø, Norway.
Nabin MallaDepartment of Medical Biology, Faculty of Health Sciences, UiT-The Arctic University of Norway, 9037 Tromsø, Norway.
Beate HeggeDepartment of Medical Biology, Faculty of Health Sciences, UiT-The Arctic University of Norway, 9037 Tromsø, Norway.
Imin WushurDepartment of Medical Biology, Faculty of Health Sciences, UiT-The Arctic University of Norway, 9037 Tromsø, Norway.
Eli BergDepartment of Medical Biology, Faculty of Health Sciences, UiT-The Arctic University of Norway, 9037 Tromsø, Norway.
Gunbjørg SvinengDepartment of Medical Biology, Faculty of Health Sciences, UiT-The Arctic University of Norway, 9037 Tromsø, Norway.
Ingebrigt SylteDepartment of Medical Biology, Faculty of Health Sciences, UiT-The Arctic University of Norway, 9037 Tromsø, Norway.ORCID 0000-0002-3290-3736
Jan-Olof WinbergDepartment of Medical Biology, Faculty of Health Sciences, UiT-The Arctic University of Norway, 9037 Tromsø, Norway.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have shown that THP-1 cells produced an SDS-stable and reduction-sensitive complex between proMMP-9 and a chondroitin sulfate proteoglycan (CSPG) core protein. The complex could be reconstituted in vitro using purified serglycin (SG) and proMMP-9 and contained no inter-disulfide bridges. It was suggested that the complex involved both the FnII module and HPX domain of proMMP-9. The aims of the present study were to resolve the interacting regions of the molecules that form the complex and the types of interactions involved. In order to study this, we expressed and purified full-length and deletion variants of proMMP-9, purified CSPG and SG, and performed in vitro reconstitution assays, peptide arrays, protein modelling, docking, and molecular dynamics (MD) simulations. ProMMP-9 variants lacking both the FnII module and the HPX domain did not form the proMMP-9∙CSPG/SG complex. Deletion variants containing at least the FnII module or the HPX domain formed the proMMP-9∙CSPG/SG complex, as did the SG core protein without CS chains. The interacting parts covered large surface areas of both molecules and implicated dynamic and complementary ionic, hydrophobic, and hydrogen bond interactions. Hence, no short single interacting linear motifs in the two macromolecules could explain the strong SDS-stable and reduction-sensitive binding.

Indexed as

Sequence DeletionAnimalsBinding SitesCell LineHumansHydrogen BondingMatrix Metalloproteinase 9Models, MolecularMolecular Docking SimulationMolecular Dynamics SimulationProtein BindingProtein ConformationProtein DomainsProteoglycansSf9 CellsTHP-1 CellsMatrix Metalloproteinase 9MMP9 protein, humanProteoglycansserglycinVesicular Transport Proteinsdockingin vitro reconstitutionmolecular dynamics simulationmolecular modellingpeptide arraysproMMP-9proMMP-9 complexesproMMP-9 deletion variantsserglycin

Identifiers

PMID32545641
PMCPMC7352350

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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.