Evidence map›Paper›PMID 22292018›Full record

ArticlePloS one2012

Suppression of p75 neurotrophin receptor surface expression with intrabodies influences Bcl-xL mRNA expression and neurite outgrowth in PC12 cells.

Congcong Zhang, Saskia Helmsing, Marta Zagrebelsky, Thomas Schirrmann, Andrea L J Marschall, Manuela Schüngel, Martin Korte, Michael Hust, Stefan Dübel

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Deletion of p75Frontiers in molecular neuroscience · 2023
    Article
  4. Article
  5. Article
  6. Recombinant Antibodies in Basic Neuroscience Research.Current protocols in neuroscience · 2020
    Review
  7. Article
  8. Applying Antibodies Inside Cells: Principles and Recent Advances in Neurobiology, Virology and Oncology.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2020
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. TAp73 knockout mice show morphological and functional nervous system defects associated with loss of p75 neurotrophin receptor.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  15. Article
  16. Article
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 2 institutions in 1 country.

Congcong ZhangInstitute for Biochemistry and Biotechnology, Technische Universität Braunschweig, Braunschweig, Germany.
Saskia Helmsing
Marta Zagrebelsky
Thomas Schirrmann
Andrea L J Marschall
Manuela Schüngel
Martin Korte
Michael Hust
Stefan Dübel
Technische Universität Braunschweig · DEMedizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlthough p75 neurotrophin receptor (p75NTR) is the first neurotrophin receptor isolated, its diverse physiological functions and signaling have remained elusive for many years. Loss-of-function phenotypic analyses for p75NTR were mainly focused at the genetic level; however these approaches were impacted by off-target effect, insufficient stability, unspecific stress response or alternative active splicing products. In this study, p75NTR surface expression was suppressed for the first time at the protein level by endoplasmic reticulum (ER) retained intrabodies.

resultsThree monoclonal recombinant antibody fragments (scFv) with affinities in the low nanomolar range to murine p75NTR were isolated by antibody phage display. To suppress p75NTR cell surface expression, the encoding genes of these scFvs extended by the ER retention peptide KDEL were transiently transfected into the neuron-like rat pheochromocytoma cell line PC12 and the mouse neuroblastoma x mouse spinal cord hybrid cell line NSC19. The ER retained intrabody construct, SH325-G7-KDEL, mediated a downregulation of p75NTR cell surface expression as shown by flow cytometry. This effect was maintained over a period of at least eight days without activating an unfolded protein response (UPR). Moreover, the ER retention of p75NTR resulted in downregulation of mRNA levels of the anti-apoptotic protein Bcl-xL as well as in strong inhibition of NGF-induced neurite outgrowth in PC12 cells.

conclusionThe ER retained intrabody SH325-G7-KDEL not only induces phenotypic knockdown of this p75NTR but also p75NTR-associated cellular responses in PC12 cells.

Indexed as

AnimalsAntibodies, MonoclonalAntigens, Surfacebcl-X ProteinCells, CulturedDown-RegulationEndoplasmic ReticulumGene Expression RegulationHEK293 CellsHumansMiceModels, BiologicalNeuritesPC12 CellsProtein TransportRatsAntibodies, MonoclonalAntigens, SurfaceBcl2l1 protein, ratbcl-X ProteinReceptor, Nerve Growth FactorRecombinant Fusion ProteinsRNA, Messenger

Identifiers

PMID22292018
PMCPMC3265506
OpenAlexW2072064103

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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.