Evidence map›Paper›PMID 23482558›Full record

ArticleThe Journal of biological chemistry2013

Notch transcriptional control of vascular smooth muscle regulatory gene expression and function.

Sanchita Basu, Dinesh Kumar Srinivasan, Ke Yang, Hema Raina, Suhanti Banerjee, Rongli Zhang, Steven A Fisher, Aaron Proweller

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Notch Signaling in Acute Inflammation and Sepsis.International journal of molecular sciences · 2023
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. "Yin and Yang" for Notch signaling in the mature vasculature.American journal of physiology. Heart and circulatory physiology · 2018
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. 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

8 authors at 1 institution in 1 country.

Sanchita BasuDepartment of Medicine, Case Cardiovascular Research Institute, Case Western Reserve University, Cleveland, Ohio 44106, USA.
Dinesh Kumar Srinivasan
Ke Yang
Hema Raina
Suhanti Banerjee
Rongli Zhang
Steven A Fisher
Aaron Proweller
Case Western Reserve University · US

Funding

SMOOTH MUSCLE MYOSIN PHOSPHATASE SUBUNIT ISOFORMSR01HL066171 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI FISHER, STEVEN A. · 2001 to 2013
$3.8M
Vascular Smooth Muscle Notch Signaling in Arterial Patterning and FunctionR01HL096603 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI PROWELLER, AARON · 2009 to 2013
$1.9M
NHLBI NIH HHS HL066171NHLBI NIH HHS HL096603NHLBI NIH HHS R01 HL066171NHLBI NIH HHS R01 HL096603
6 · The paper itself

Abstract

Notch receptors and ligands mediate heterotypic cell signaling that is required for normal vascular development. Dysregulation of select Notch receptors in mouse vascular smooth muscle (VSM) and in genetic human syndromes causes functional impairment in some regional circulations, the mechanistic basis of which is undefined. In this study, we used a dominant-negative Mastermind-like (DNMAML1) to block signaling through all Notch receptors specifically in VSM to more broadly test a functional role for this pathway in vivo. Mutant DNMAML1-expressing mice exhibited blunted blood pressure responses to vasoconstrictors, and their aortic, femoral, and mesenteric arteries had reduced contractile responses to agonists and depolarization in vitro. The mutant arteries had significant and specific reduction in the expression and activity of myosin light chain kinase (MLCK), a primary regulator of VSM force production. Conversely, activated Notch signaling in VSM cells induced endogenous MLCK transcript levels. We identified MLCK as a direct target of activated Notch receptor as demonstrated by an evolutionarily conserved Notch-responsive element within the MLCK promoter that binds the Notch receptor complex and is required for transcriptional activity. We conclude that Notch signaling through the transcriptional control of key regulatory proteins is required for contractile responses of mature VSM. Genetic or pharmacological manipulation of Notch signaling is a potential strategy for modulating arterial function in human disease.

Indexed as

Gene Expression RegulationSignal TransductionAnimalsGenetic Diseases, InbornHumansMiceMice, TransgenicMuscle ContractionMuscle ProteinsMuscle, Smooth, VascularMyosin-Light-Chain KinaseNuclear ProteinsReceptors, NotchTranscription FactorsTranscription, GeneticVascular DiseasesMaml1 protein, mouseMuscle ProteinsMyosin-Light-Chain KinaseNuclear ProteinsReceptors, NotchTranscription Factors

Identifiers

PMID23482558
PMCPMC3630855
OpenAlexW2037753075

What OpenQuestion holds

Textmetadata
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.