Evidence map›Paper›PMID 28499450›Full record

ArticleBMC biotechnology2017

Intrabodies against the Polysialyltransferases ST8SiaII and ST8SiaIV inhibit Polysialylation of NCAM in rhabdomyosarcoma tumor cells.

Stefan Somplatzki, Martina Mühlenhoff, Andrea Kröger, Rita Gerardy-Schahn, Thomas Böldicke

Open access · goldAbstract read
In one paragraph

Article in BMC biotechnology, 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
1.3field-weighted citation impact, top 20% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
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  4. Applying Antibodies Inside Cells: Principles and Recent Advances in Neurobiology, Virology and Oncology.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2020
    Review
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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

5 authors at 2 institutions in 1 country.

Stefan SomplatzkiHelmholtz Centre for Infection Research, Structural and Functional Protein Research, Inhoffenstraße 7, D-38124, Braunschweig, Germany.
Martina MühlenhoffInstitute of Cellular Chemistry, Hannover Medical School, D-30625, Hannover, Germany.
Andrea KrögerHelmholtz Centre for Infection Research, Group Innate Immunity and Infection, Inhoffenstraße 7, D-38124, Braunschweig, Germany.
Rita Gerardy-SchahnInstitute of Cellular Chemistry, Hannover Medical School, D-30625, Hannover, Germany.
Thomas BöldickeHelmholtz Centre for Infection Research, Structural and Functional Protein Research, Inhoffenstraße 7, D-38124, Braunschweig, Germany. thomas.boeldicke@helmholtz-hzi.de.
Helmholtz Centre for Infection Research · DEMedizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPolysialic acid (polySia) is a carbohydrate modification of the neural cell adhesion molecule (NCAM), which is implicated in neural differentiation and plays an important role in tumor development and metastasis. Polysialylation of NCAM is mediated by two Golgi-resident polysialyltransferases (polyST) ST8SiaII and ST8SiaIV. Intracellular antibodies (intrabodies; IB) expressed inside the ER and retaining proteins passing the ER such as cell surface receptors or secretory proteins provide an efficient means of protein knockdown. To inhibit the function of ST8SiaII and ST8SiaIV specific ER IBs were generated starting from two corresponding hybridoma clones. Both IBs αST8SiaII-IB and αST8SiaIV-IB were constructed in the scFv format and their functions characterized in vitro and in vivo.

resultsIBs directed against the polySTs prevented the translocation of the enzymes from the ER to the Golgi-apparatus. Co-immunoprecipitation of ST8SiaII and ST8SiaIV with the corresponding IBs confirmed the intracellular interaction with their cognate antigens. In CHO cells overexpressing ST8SiaII and ST8SiaIV, respectively, the transfection with αST8SiaII-IB or αST8SiaIV-IB inhibited significantly the cell surface expression of polysialylated NCAM. Furthermore stable expression of ST8SiaII-IB, ST8SiaIV-IB and luciferase in the rhabdomyosarcoma cell line TE671 reduced cell surface expression of polySia and delayed tumor growth if cells were xenografted into C57BL/6 J RAG-2 mice.

conclusionData obtained strongly indicate that αST8SiaII-IB and αST8SiaIV-IB are promising experimental tools to analyze the individual role of the two enzymes during brain development and during migration and proliferation of tumor cells.

Indexed as

AnimalsAntibodiesBase SequenceCell Line, TumorCHO CellsCricetinaeCricetulusEndoplasmic ReticulumHEK293 CellsHumansImmunoprecipitationMiceMice, Inbred C57BLMicroscopy, FluorescenceNeural Cell Adhesion MoleculesPlasmidsAntibodiesNeural Cell Adhesion Moleculespolysialic acidSialic AcidsSialyltransferasesER intrabodiesNeural cell adhesion moleculePolysialic acid cell surface expressionPolysialyltransferasesXenograft tumor mouse model

Identifiers

PMID28499450
PMCPMC5429572
OpenAlexW2612138996

What OpenQuestion holds

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LicenceCC BY
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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.