Evidence map›Paper›PMID 24285540›Full record

ArticleThe Journal of biological chemistry2014

Mechanoregulation of h2-calponin gene expression and the role of Notch signaling.

Wen-rui Jiang, Geoffrey Cady, M Moazzem Hossain, Qi-Quan Huang, Xin Wang, J-P Jin

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Evolution and function of calponin and transgelin.Frontiers in cell and developmental biology · 2023
    Review
  6. Article
  7. Downregulation of calponin 2 contributes to the quiescence of lung macrophages.American journal of physiology. Cell physiology · 2019
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. 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 1 institution in 1 country.

Wen-rui JiangFrom the Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan 48201.
Geoffrey Cady
M Moazzem Hossain
Qi-Quan Huang
Xin Wang
J-P Jin
Wayne State University · US

Funding

Regulation & Function of CalponinR01HL086720 · NHLBI · WAYNE STATE UNIVERSITY · PI JIN, JIAN-PING · 2007 to 2010
$1.5M
NHLBI NIH HHS HL-086720NHLBI NIH HHS R01 HL086720
6 · The paper itself

Abstract

The essential role of mechanical signals in regulating the function of living cells is universally observed. However, how mechanical signals are transduced in cells to regulate gene expression is largely unknown. We previously demonstrated that the gene encoding h2-calponin (Cnn2) is sensitively regulated by mechanical tension. In the present study, mouse genomic DNA containing the Cnn2 promoter was cloned, and a nested set of 5' truncations was studied. Transcriptional activity of the Cnn2 promoter-reporter constructs was examined in transfected NIH/3T3, HEK293, and C2C12 cells for their responses to the stiffness of culture substrate. The results showed significant transcriptional activities of the -1.00- and -1.24-kb promoter constructs, whereas the -0.61-kb construct was inactive. The -1.38-, -1.57-, and -2.12-kb constructs showed higher transcriptional activity, whereas only the -1.57- and -2.12-kb constructs exhibited repression of expression when the host cells were cultured on low stiffness substrate. Internal deletion of the segment between -1.57 and -1.38 kb in the -2.12-kb promoter construct abolished the low substrate stiffness-induced repression. Site-specific deletion or mutation of an HES-1 transcription factor binding site in this region also abolished this repression effect. The level of HES-1 increased in cells cultured under a low tension condition, corresponding to the down-regulation of h2-calponin. h2-Calponin gene expression is further affected by the treatment of cells with Notch inhibitor and activator, suggesting an upstream signaling mechanism.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsCalcium-Binding ProteinsCalponinsGene DeletionGene Expression RegulationHEK293 CellsHomeodomain ProteinsHumansK562 CellsMiceMicrofilament ProteinsNIH 3T3 CellsPromoter Regions, GeneticReceptors, NotchSignal TransductionBasic Helix-Loop-Helix ProteinsCalcium-Binding ProteinsCalponinsHES1 protein, humanHes1 protein, mouseHomeodomain ProteinsMicrofilament ProteinsReceptors, NotchTranscription Factor HES-1ActinCell BiologyGene TranscriptionMechanotransductionTranscription Promoter

Identifiers

PMID24285540
PMCPMC3894341
OpenAlexW2076754423

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.