Evidence map›Paper›PMID 28927755›Full record

ArticleVascular pharmacology2017

Protein kinase CK2 inhibition suppresses neointima formation via a proline-rich homeodomain-dependent mechanism.

K S Wadey, B A Brown, G B Sala-Newby, P-S Jayaraman, K Gaston, S J George

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Vascular pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

5 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Inhibition of Intimal Thickening By PRH (Proline-Rich Homeodomain) in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2023
    Article
  3. Targeting protein kinase CK2 in the treatment of cholangiocarcinoma.Exploration of targeted anti-tumor therapy · 2021
    Review
  4. Article
  5. 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

6 authors at 3 institutions in 1 country.

K S WadeySchool of Clinical Sciences, University of Bristol, Research Floor Level 7, Bristol Royal Infirmary, Bristol BS2 8HW, UK; Department of Biochemistry, University of Bristol, Bristol BS8 1TD, UK.
B A BrownSchool of Clinical Sciences, University of Bristol, Research Floor Level 7, Bristol Royal Infirmary, Bristol BS2 8HW, UK.
G B Sala-NewbySchool of Clinical Sciences, University of Bristol, Research Floor Level 7, Bristol Royal Infirmary, Bristol BS2 8HW, UK.
P-S JayaramanDivision of Immunity and Infection, College of Medicine, University Birmingham, Edgbaston, Birmingham B15 2TT, UK.
K GastonDepartment of Biochemistry, University of Bristol, Bristol BS8 1TD, UK.
S J GeorgeSchool of Clinical Sciences, University of Bristol, Research Floor Level 7, Bristol Royal Infirmary, Bristol BS2 8HW, UK. Electronic address: s.j.george@bristol.ac.uk.
Bristol Royal Infirmary · GBUniversity of Birmingham · GBUniversity of Bristol · GB

Funding

British Heart Foundation FS/10/58/28515Medical Research Council MR/N012615/1
6 · The paper itself

Abstract

Neointimal hyperplasia is a product of VSMC replication and consequent accumulation within the blood vessel wall. In this study, we determined whether inhibition of protein kinase CK2 and the resultant stabilisation of proline-rich homeodomain (PRH) could suppress VSMC proliferation. Both silencing and pharmacological inhibition of CK2 with K66 antagonised replication of isolated VSMCs. SiRNA-induced knockdown as well as ectopic overexpression of proline-rich homeodomain indicated that PRH disrupts cell cycle progression. Mutation of CK2 phosphorylation sites Ser

Indexed as

NeointimaAnimalsCasein Kinase IICell Cycle CheckpointsCell ProliferationCells, CulturedHomeodomain ProteinsHumansHuman Umbilical Vein Endothelial CellsHyperplasiaMuscle, Smooth, VascularMutationMyocytes, Smooth MusclePhosphorylationProline-Rich Protein DomainsProtein Kinase InhibitorsCasein Kinase IICSNK2A1 protein, humanHHEX protein, humanHhex protein, ratHomeodomain ProteinsProtein Kinase InhibitorsTranscription FactorsAtherosclerosisCK2In-stent restenosisPRHVascular smooth muscleVein graft

Identifiers

PMID28927755
PMCPMC5718878
OpenAlexW2754990616

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.