Evidence map›Paper›PMID 27189939›Full record

ArticleThe Journal of biological chemistry2016

Crystal Structure of a Two-domain Fragment of Hepatocyte Growth Factor Activator Inhibitor-1: FUNCTIONAL INTERACTIONS BETWEEN THE KUNITZ-TYPE INHIBITOR DOMAIN-1 AND THE NEIGHBORING POLYCYSTIC KIDNEY DISEASE-LIKE DOMAIN.

Zebin Hong, Laura De Meulemeester, Annemarie Jacobi, Jan Skov Pedersen, J Preben Morth, Peter A Andreasen, Jan K Jensen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

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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

7 authors at 2 institutions in 2 countries.

Zebin HongDepartment of Molecular Biology and Genetics, Danish-Chinese Centre for Proteases and Cancer, Aarhus University, Gustav Wieds Vej 10C, 8000 Aarhus C, Denmark.
Laura De MeulemeesterDepartment of Molecular Biology and Genetics, Danish-Chinese Centre for Proteases and Cancer, Aarhus University, Gustav Wieds Vej 10C, 8000 Aarhus C, Denmark.
Annemarie JacobiDepartment of Molecular Biology and Genetics, Danish-Chinese Centre for Proteases and Cancer, Aarhus University, Gustav Wieds Vej 10C, 8000 Aarhus C, Denmark.
Jan Skov PedersenDepartment of Chemistry and iNANO Interdisciplinary Nanoscience Center, Aarhus University, 8000 Aarhus C, Denmark.
J Preben MorthNorwegian Center of Molecular Medicine (NCMM), University of Oslo, NO-0316 Oslo, Norway.
Peter A AndreasenDepartment of Molecular Biology and Genetics, Danish-Chinese Centre for Proteases and Cancer, Aarhus University, Gustav Wieds Vej 10C, 8000 Aarhus C, Denmark.
Jan K JensenDepartment of Molecular Biology and Genetics, Danish-Chinese Centre for Proteases and Cancer, Aarhus University, Gustav Wieds Vej 10C, 8000 Aarhus C, Denmark,. Electronic address: jkj@mbg.au.dk.
Aarhus University · DKUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocyte growth factor activator inhibitor-1 (HAI-1) is a type I transmembrane protein and inhibitor of several serine proteases, including hepatocyte growth factor activator and matriptase. The protein is essential for development as knock-out mice die in utero due to placental defects caused by misregulated extracellular proteolysis. HAI-1 contains two Kunitz-type inhibitor domains (Kunitz), which are generally thought of as a functionally self-contained protease inhibitor unit. This is not the case for HAI-1, where our results reveal how interdomain interactions have evolved to stimulate the inhibitory activity of an integrated Kunitz. Here we present an x-ray crystal structure of an HAI-1 fragment covering the internal domain and Kunitz-1. The structure reveals not only that the previously uncharacterized internal domain is a member of the polycystic kidney disease domain family but also how the two domains engage in interdomain interactions. Supported by solution small angle x-ray scattering and a combination of site-directed mutagenesis and functional assays, we show that interdomain interactions not only stabilize the fold of the internal domain but also stimulate the inhibitory activity of Kunitz-1. By completing our structural characterization of the previously unknown N-terminal region of HAI-1, we provide new insight into the interplay between tertiary structure and the inhibitory activity of a multidomain protease inhibitor. We propose a previously unseen mechanism by which the association of an auxiliary domain stimulates the inhibitory activity of a Kunitz-type inhibitor (i.e. the first structure of an intramolecular interaction between a Kunitz and another domain).

Indexed as

Amino Acid SequenceAnimalsCrystallography, X-RayMembrane GlycoproteinsMiceMice, KnockoutModels, MolecularMolecular Sequence DataPolycystic Kidney DiseasesProteinase Inhibitory Proteins, SecretoryProtein BindingProtein ConformationRecombinant ProteinsScattering, Small AngleSequence Homology, Amino AcidSurface Plasmon ResonanceMembrane GlycoproteinsProteinase Inhibitory Proteins, SecretoryRecombinant ProteinsSpint1 protein, mousecell surface proteininhibition mechanismmultidomain proteinprotease inhibitorprotein-protein interactiontertiary structure

Identifiers

PMID27189939
PMCPMC4933187
OpenAlexW2345596619

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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.