Evidence map›Paper›PMID 23455440›Full record

ArticleActa neuropathologica2013

Epigenetic regulation of cholinergic receptor M1 (CHRM1) by histone H3K9me3 impairs Ca(2+) signaling in Huntington's disease.

Junghee Lee, Yu Jin Hwang, Jong-Yeon Shin, Won-Chul Lee, Jinhong Wie, Ki Yoon Kim, Min Young Lee, Daehee Hwang, Rajiv R Ratan, Ae Nim Pae and 4 more

Abstract read
In one paragraph

Article in Acta neuropathologica, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.1field-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

27 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
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  9. Article
  10. Phospho-Tau and Chromatin Landscapes in Early and Late Alzheimer's Disease.International journal of molecular sciences · 2021
    Review
  11. Epigenetic regulation in Huntington's disease.Neurochemistry international · 2021
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. The epigenetics of aging and neurodegeneration.Progress in neurobiology · 2015
    Review
  20. 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

14 authors at 6 institutions in 2 countries.

Junghee LeeVeteran's Affairs Boston Healthcare System, Boston, MA 02130, USA.
Yu Jin Hwang
Jong-Yeon Shin
Won-Chul Lee
Jinhong Wie
Ki Yoon Kim
Min Young Lee
Daehee Hwang
Rajiv R Ratan
Ae Nim Pae
Neil W Kowall
Insuk So
Jong-Il Kim
Hoon Ryu
Seoul National University · KRPohang University of Science and Technology · KRVA Boston Healthcare System · USBurke Medical Research Institute · USIo Therapeutics (United States) · USKorea Institute of Brain Science · KR

Funding

TRANSCRIPTIONAL RESPONSES TO MITOCHONDRIAL DYSFUNCTIONP01AG014930 · NIA · WINIFRED MASTERSON BURKE MED RES INST · PI GIBSON, GARY E · 1999 to 2020
$30.7M
Neuropathology CoreP30AG013846 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI KOWALL, NEIL W. · 1996 to 2020
$29.1M
Epigenetic Regulation of Heterochromatin Condensation in Huntington's DiseaseR01NS067283 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI RYU, HOON · 2011 to 2015
$1.2M
NIA NIH HHS P01 AG014930NIA NIH HHS P30 AG013846NINDS NIH HHS R01 NS067283
6 · The paper itself

Abstract

Huntington's disease (HD) is an autosomal dominant neurodegenerative disease caused by an expanded trinucleotide CAG repeat in the gene coding for huntingtin. Deregulation of chromatin remodeling is linked to the pathogenesis of HD but the mechanism remains elusive. To identify what genes are deregulated by trimethylated histone H3K9 (H3K9me3)-dependent heterochromatin, we performed H3K9me3-ChIP genome-wide sequencing combined with RNA sequencing followed by platform integration analysis in stable striatal HD cell lines (STHdhQ7/7 and STHdhQ111/111) cells. We found that genes involving neuronal synaptic transmission including cholinergic receptor M1 (CHRM1), cell motility, and neuronal differentiation pathways are downregulated while their promoter regions are highly occupied with H3K9me3 in HD. Moreover, we found that repression of CHRM1 gene expression by H3K9me3 impairs Ca(2+)-dependent neuronal signal transduction in stable cell lines expressing mutant HD protein. Thus, our data indicate that the epigenetic modifications, such as aberrant H3K9me3-dependent heterochromatin plasticity, directly contribute to the pathogenesis of HD.

Indexed as

AnimalsCalcium SignalingDisease Models, AnimalEpigenesis, GeneticFemaleHistonesHumansHuntingtin ProteinHuntington DiseaseMiceNerve Tissue ProteinsNeuronal PlasticityPromoter Regions, GeneticReceptor, Muscarinic M1Receptors, MuscarinicRNA, MessengerCHRM1 protein, humanHistonesHTT protein, humanHuntingtin ProteinNerve Tissue ProteinsReceptor, Muscarinic M1Receptors, MuscarinicRNA, Messenger

Identifiers

PMID23455440
PMCPMC3633717
OpenAlexW2042293684

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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.