Evidence map›Paper›PMID 25827571›Full record

ArticleMolecular & cellular proteomics : MCP2015

Secretome analysis identifies novel signal Peptide peptidase-like 3 (Sppl3) substrates and reveals a role of Sppl3 in multiple Golgi glycosylation pathways.

Peer-Hendrik Kuhn, Matthias Voss, Martina Haug-Kröper, Bernd Schröder, Ute Schepers, Stefan Bräse, Christian Haass, Stefan F Lichtenthaler, Regina Fluhrer

Open access · hybridAbstract read
In one paragraph

Article in Molecular & cellular proteomics : MCP, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

  1. Pooled it
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  12. Genome-Wide Identification of the SPP/SPPL Gene Family andInternational journal of molecular sciences · 2024
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  15. iScience · 2023
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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

9 authors at 5 institutions in 1 country.

Peer-Hendrik KuhnFrom the DZNE - German Center for Neurodegenerative Diseases, Munich, Germany; Institute for Advanced Study, Technische Universität München, Garching, Germany;
Matthias VossInstitute for Metabolic Biochemistry, Ludwig-Maximilians University Munich, Munich, Germany;
Martina Haug-KröperInstitute for Metabolic Biochemistry, Ludwig-Maximilians University Munich, Munich, Germany;
Bernd SchröderBiochemical Institute, Christian-Albrechts University Kiel, Olshausenstrasse 40, D-24118 Kiel, Germany;
Ute SchepersInstitute of Toxicology and Genetics, KIT, Campus North, Hermann-von-Helmholtz-Platz 1, D-76344 Eggenstein-Leopoldshafen, Germany Munich Cluster for Systems Neurology (SyNergy), Munich, Germany;
Stefan BräseInstitute of Toxicology and Genetics, KIT, Campus North, Hermann-von-Helmholtz-Platz 1, D-76344 Eggenstein-Leopoldshafen, Germany Munich Cluster for Systems Neurology (SyNergy), Munich, Germany;
Christian HaassFrom the DZNE - German Center for Neurodegenerative Diseases, Munich, Germany; Institute for Metabolic Biochemistry, Ludwig-Maximilians University Munich, Munich, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany;
Stefan F LichtenthalerFrom the DZNE - German Center for Neurodegenerative Diseases, Munich, Germany; Institute for Advanced Study, Technische Universität München, Garching, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany; Neuroproteomics, Klinikum rechts der Isar, Technische Universität München, Munich, Germany.
Regina FluhrerFrom the DZNE - German Center for Neurodegenerative Diseases, Munich, Germany; Institute for Metabolic Biochemistry, Ludwig-Maximilians University Munich, Munich, Germany; regina.fluhrer@med.uni-muenchen.de stefan.lichtenthaler@dzne.de.
Ludwig-Maximilians-Universität München · DEGerman Center for Neurodegenerative Diseases · DEMunich Cluster for Systems Neurology · DEKiel University · DETechnical University of Munich · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Signal peptide peptidase-like 3 (Sppl3) is a Golgi-resident intramembrane-cleaving protease that is highly conserved among multicellular eukaryotes pointing to pivotal physiological functions in the Golgi network which are only beginning to emerge. Recently, Sppl3 was shown to control protein N-glycosylation, when the key branching enzyme N-acetylglucosaminyltransferase V (GnT-V) and other medial/trans Golgi glycosyltransferases were identified as first physiological Sppl3 substrates. Sppl3-mediated endoproteolysis releases the catalytic ectodomains of these enzymes from their type II membrane anchors. Protein glycosylation is a multistep process involving numerous type II membrane-bound enzymes, but it remains unclear whether only few of them are Sppl3 substrates or whether Sppl3 cleaves many of them and thereby controls protein glycosylation at multiple levels. Therefore, to systematically identify Sppl3 substrates we used Sppl3-deficient and Sppl3-overexpression cell culture models and analyzed them for changes in secreted membrane protein ectodomains using the proteomics "secretome protein enrichment with click sugars (SPECS)" method. SPECS analysis identified numerous additional new Sppl3 candidate glycoprotein substrates, several of which were biochemically validated as Sppl3 substrates. All novel Sppl3 substrates adopt a type II topology. The majority localizes to the Golgi network and is implicated in Golgi functions. Importantly, most of the novel Sppl3 substrates catalyze the modification of N-linked glycans. Others contribute to O-glycan and in particular glycosaminoglycan biosynthesis, suggesting that Sppl3 function is not restricted to N-glycosylation, but also functions in other forms of protein glycosylation. Hence, Sppl3 emerges as a crucial player of Golgi function and the newly identified Sppl3 substrates will be instrumental to investigate the molecular mechanisms underlying the physiological function of Sppl3 in the Golgi network and in vivo. Data are available via ProteomeXchange with identifier PXD001672.

Indexed as

Aspartic Acid EndopeptidasesGlycosylationGolgi ApparatusHEK293 CellsHumansAspartic Acid Endopeptidasessignal peptide peptidase like 3, human

Identifiers

PMID25827571
PMCPMC4458722
OpenAlexW2063027721

What OpenQuestion holds

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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.