Evidence map›Paper›PMID 36012764›Full record

ArticleInternational journal of molecular sciences2022

CDNF Interacts with ER Chaperones and Requires UPR Sensors to Promote Neuronal Survival.

Ave Eesmaa, Li-Ying Yu, Helka Göös, Tatiana Danilova, Kristofer Nõges, Emmi Pakarinen, Markku Varjosalo, Maria Lindahl, Päivi Lindholm, Mart Saarma

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

11 citing papers in PubMed, 30 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

10 authors at 1 institution in 1 country.

Ave EesmaaInstitute of Biotechnology, HiLIFE, University of Helsinki, 00790 Helsinki, Finland.
Li-Ying YuInstitute of Biotechnology, HiLIFE, University of Helsinki, 00790 Helsinki, Finland.
Helka GöösInstitute of Biotechnology, HiLIFE, University of Helsinki, 00790 Helsinki, Finland.
Tatiana DanilovaInstitute of Biotechnology, HiLIFE, University of Helsinki, 00790 Helsinki, Finland.
Kristofer NõgesInstitute of Biotechnology, HiLIFE, University of Helsinki, 00790 Helsinki, Finland.
Emmi PakarinenInstitute of Biotechnology, HiLIFE, University of Helsinki, 00790 Helsinki, Finland.
Markku VarjosaloInstitute of Biotechnology, HiLIFE, University of Helsinki, 00790 Helsinki, Finland.ORCID 0000-0002-1340-9732
Maria LindahlInstitute of Biotechnology, HiLIFE, University of Helsinki, 00790 Helsinki, Finland.ORCID 0000-0002-5674-8830
Päivi LindholmInstitute of Biotechnology, HiLIFE, University of Helsinki, 00790 Helsinki, Finland.ORCID 0000-0003-3022-5035
Mart SaarmaInstitute of Biotechnology, HiLIFE, University of Helsinki, 00790 Helsinki, Finland.ORCID 0000-0001-5543-7160
University of Helsinki · FI

Funding

Academy of Finland 117044Academy of Finland 343299Jane and Aatos Erkko Foundation 12-112433-12
6 · The paper itself

Abstract

Cerebral dopamine neurotrophic factor (CDNF) is a neurotrophic factor that has beneficial effects on dopamine neurons in both in vitro and in vivo models of Parkinson's disease (PD). CDNF was recently tested in phase I-II clinical trials for the treatment of PD, but the mechanisms underlying its neuroprotective properties are still poorly understood, although studies have suggested its role in the regulation of endoplasmic reticulum (ER) homeostasis and the unfolded protein response (UPR). The aim of this study was to investigate the mechanism of action of CDNF through analyzing the involvement of UPR signaling in its anti-apoptotic function. We used tunicamycin to induce ER stress in mice in vivo and used cultured primary neurons and found that CDNF expression is regulated by ER stress in vivo and that the involvement of UPR pathways is important for the neuroprotective function of CDNF. Moreover, we used AP-MS and BiFC to perform the first interactome screening for CDNF and report novel binding partners of CDNF. These findings allowed us to hypothesize that CDNF protects neurons from ER-stress-inducing agents by modulating UPR signaling towards cell survival outcomes.

Indexed as

Molecular ChaperonesNerve Growth FactorsParkinson DiseaseAnimalsCell SurvivalDopaminergic NeuronsEndoplasmic ReticulumEndoplasmic Reticulum StressMiceUnfolded Protein Responsecdnf protein, mouseMolecular ChaperonesNerve Growth FactorsapoptosisCDNFdopamine neuronsER stressmechanism of actionneurotrophic factorprotein–protein interactionssympathetic neuronsunfolded protein response

Identifiers

PMID36012764
PMCPMC9408947
OpenAlexW4292687711

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.