Evidence map›Paper›PMID 20075068›Full record

ArticleThe Journal of biological chemistry2010

Stefin B interacts with histones and cathepsin L in the nucleus.

Slavko Čeru, Špela Konjar, Katarina Maher, Urška Repnik, Igor Križaj, Mojca Benčina, Miha Renko, Alain Nepveu, Eva Žerovnik, Boris Turk and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

46 citing papers in PubMed, 96 citations in OpenAlex.

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  19. Expression of Cathepsin L and Its Intrinsic Inhibitors in Glomeruli of Rats With Puromycin Aminonucleoside Nephrosis.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2018
    Article
  20. Cathepsins: Proteases that are vital for survival but can also be fatal.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2018
    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

11 authors at 3 institutions in 2 countries.

Slavko ČeruDepartments of Biochemistry and Molecular and Structural Biology, Ljubljana SI-1000, Slovenia.
Špela KonjarDepartments of Biochemistry and Molecular and Structural Biology, Ljubljana SI-1000, Slovenia.
Katarina MaherDepartments of Biochemistry and Molecular and Structural Biology, Ljubljana SI-1000, Slovenia.
Urška RepnikDepartments of Biochemistry and Molecular and Structural Biology, Ljubljana SI-1000, Slovenia.
Igor KrižajMolecular and Biomedical Sciences, Jožef Stefan Institute, Ljubljana SI-1000, Slovenia.
Mojca BenčinaDepartment of Biotechnology, National Institute of Chemistry, Ljubljana SI-1000, Slovenia.
Miha RenkoDepartments of Biochemistry and Molecular and Structural Biology, Ljubljana SI-1000, Slovenia.
Alain NepveuMolecular Oncology Group, McGill University, Montreal, Quebec H3A 1A1, Canada.
Eva ŽerovnikDepartments of Biochemistry and Molecular and Structural Biology, Ljubljana SI-1000, Slovenia.
Boris TurkDepartments of Biochemistry and Molecular and Structural Biology, Ljubljana SI-1000, Slovenia.
Nataša Kopitar-JeralaDepartments of Biochemistry and Molecular and Structural Biology, Ljubljana SI-1000, Slovenia. Electronic address: natasa.kopitar@ijs.si.
Jožef Stefan Institute · SIMcGill University · CANational Institute of Chemistry · SI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stefin B (cystatin B) is an endogenous inhibitor of cysteine proteinases localized in the nucleus and the cytosol. Loss-of-function mutations in the stefin B gene (CSTB) gene were reported in patients with Unverricht-Lundborg disease (EPM1). We have identified an interaction between stefin B and nucleosomes, specifically with histones H2A.Z, H2B, and H3. In synchronized T98G cells, stefin B co-immunoprecipitated with histone H3, predominantly in the G(1) phase of the cell cycle. Stefin B-deficient mouse embryonic fibroblasts entered S phase earlier than wild type mouse embryonic fibroblasts. In contrast, increased expression of stefin B in the nucleus delayed cell cycle progression in T98G cells. The delay in cell cycle progression was associated with the inhibition of cathepsin L in the nucleus, as judged from the decreased cleavage of the CUX1 transcription factor. In vitro, inhibition of cathepsin L by stefin B was potentiated in the presence of histones, whereas histones alone did not affect the cathepsin L activity. Interaction of stefin B with the Met-75 truncated form of cathepsin L in the nucleus was confirmed by fluorescence resonance energy transfer experiments in the living cells. Stefin B could thus play an important role in regulating the proteolytic activity of cathepsin L in the nucleus, protecting substrates such as transcription factors from its proteolytic processing.

Indexed as

Gene Expression RegulationAnimalsCathepsin LCell CycleCell Line, TumorCell NucleusCystatin BCytosolFibroblastsFluorescence Resonance Energy TransferHistonesHumansMiceModels, BiologicalCathepsin LCystatin BHistones

Identifiers

PMID20075068
PMCPMC2843170
OpenAlexW2161500231

What OpenQuestion holds

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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.