Evidence map›Paper›PMID 30008670›Full record

ArticleFrontiers in pharmacology2018

Patient-Specific iPSC-Based Models of Huntington's Disease as a Tool to Study Store-Operated Calcium Entry Drug Targeting.

Vladimir Vigont, Evgeny Nekrasov, Alexey Shalygin, Konstantin Gusev, Sergey Klushnikov, Sergey Illarioshkin, Maria Lagarkova, Sergey L Kiselev, Elena Kaznacheyeva

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  5. Direct Reprogramming of Somatic Skin Cells from a Patient with Huntington's Disease into Striatal Neurons to Create Models of Pathology.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2024
    Article
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  15. Article
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  19. Frontiers in cell and developmental biology · 2020
    Review
  20. Modeling Polyglutamine Expansion Diseases with Induced Pluripotent Stem Cells.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019
    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

9 authors at 4 institutions in 1 country.

Vladimir VigontInstitute of Cytology, Russian Academy of Sciences, Saint Petersburg, Russia.
Evgeny NekrasovVavilov Institute of General Genetics, Russian Academy of Sciences, Moscow, Russia.
Alexey ShalyginInstitute of Cytology, Russian Academy of Sciences, Saint Petersburg, Russia.
Konstantin GusevInstitute of Cytology, Russian Academy of Sciences, Saint Petersburg, Russia.
Sergey KlushnikovScientific Center of Neurology, Russian Academy of Medical Sciences, Moscow, Russia.
Sergey IllarioshkinScientific Center of Neurology, Russian Academy of Medical Sciences, Moscow, Russia.
Maria LagarkovaVavilov Institute of General Genetics, Russian Academy of Sciences, Moscow, Russia.
Sergey L KiselevVavilov Institute of General Genetics, Russian Academy of Sciences, Moscow, Russia.
Elena KaznacheyevaInstitute of Cytology, Russian Academy of Sciences, Saint Petersburg, Russia.
Institute of Cytology · RUResearch Center of Neurology · RUVavilov Institute of General Genetics · RUResearch Institute of Physical Chemical Medicine · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurodegenerative pathologies are among the most serious and socially significant problems of modern medicine, along with cardiovascular and oncological diseases. Several attempts have been made to prevent neuronal death using novel drugs targeted to the cell calcium signaling machinery, but the lack of adequate models for screening markedly impairs the development of relevant drugs. A potential breakthrough in this field is offered by the models of hereditary neurodegenerative pathologies based on endogenous expression of mutant proteins in neurons differentiated from patient-specific induced pluripotent stem cells (iPSCs). Here, we study specific features of store-operated calcium entry (SOCE) using an iPSCs-based model of Huntington's disease (HD) and analyze the pharmacological effects of a specific drug targeted to the calcium channels. We show that SOCE in gamma aminobutyric acid-ergic striatal medium spiny neurons (GABA MSNs) was mediated by currents through at least two different channel groups,

Indexed as

CRAC channelsEVP4593Huntington’s diseaseiPS cellsneurodegenerationSOCstore-operated calcium channels

Identifiers

PMID30008670
PMCPMC6033963
OpenAlexW2807224704

What Socratic 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 Socratic graph.