Evidence map›Paper›PMID 24151072›Full record

ArticleThe Journal of biological chemistry2013

Regulation of 130-kDa smooth muscle myosin light chain kinase expression by an intronic CArG element.

Meng Chen, Wenwu Zhang, Xiao Lu, April M Hoggatt, Susan J Gunst, Ghassan S Kassab, Johnathan D Tune, B Paul Herring

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 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. Myosin Light-Chain Kinase Inhibition Potentiates the Antitumor Effects of Avapritinib in PDGFRA D842V-Mutant Gastrointestinal Stromal Tumor.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
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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 2 institutions in 1 country.

Meng ChenFrom the Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana 46202.
Wenwu Zhang
Xiao Lu
April M Hoggatt
Susan J Gunst
Ghassan S Kassab
Johnathan D Tune
B Paul Herring
Indiana University Bloomington · USIndiana University – Purdue University Indianapolis · US

Funding

Function of the 130kDa MLCK in vasculature physiology and pathophysiologyR01HL085212 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI HERRING, BRIAN PAUL · 2009 to 2010
$718k
NHLBI NIH HHS HL085212NHLBI NIH HHS R01 HL085212
6 · The paper itself

Abstract

The mylk1 gene encodes a 220-kDa nonmuscle myosin light chain kinase (MLCK), a 130-kDa smooth muscle MLCK (smMLCK), as well as the non-catalytic product telokin. Together, these proteins play critical roles in regulating smooth muscle contractility. Changes in their expression are associated with many pathological conditions; thus, it is important to understand the mechanisms regulating expression of mylk1 gene transcripts. Previously, we reported a highly conserved CArG box, which binds serum response factor, in intron 15 of mylk1. Because this CArG element is near the promoter that drives transcription of the 130-kDa smMLCK, we examined its role in regulating expression of this transcript. Results show that deletion of the intronic CArG region from a β-galactosidase reporter gene abolished transgene expression in mice in vivo. Deletion of the CArG region from the endogenous mylk1 gene, specifically in smooth muscle cells, decreased expression of the 130-kDa smMLCK by 40% without affecting expression of the 220-kDa MLCK or telokin. This reduction in 130-kDa smMLCK expression resulted in decreased phosphorylation of myosin light chains, attenuated smooth muscle contractility, and a 24% decrease in small intestine length that was associated with a significant reduction of Ki67-positive smooth muscle cells. Overall, these data show that the CArG element in intron 15 of the mylk1 gene is necessary for maximal expression of the 130-kDa smMLCK and that the 130-kDa smMLCK isoform is specifically required to regulate smooth muscle contractility and small intestine smooth muscle cell proliferation.

Indexed as

AnimalsCell ProliferationGene Expression RegulationHeterogeneous-Nuclear Ribonucleoprotein Group A-BIntronsKi-67 AntigenMiceMuscle ContractionMyocytes, Smooth MuscleMyosin-Light-Chain KinasePromoter Regions, GeneticProtein BindingProtein IsoformsRepressor ProteinsSerum Response FactorHeterogeneous-Nuclear Ribonucleoprotein Group A-BHnrnpab protein, mouseKi-67 AntigenMyosin-Light-Chain KinaseProtein IsoformsRepressor ProteinsSerum Response FactorCalcium Calmodulin-dependent Protein Kinase (CaMK)Contractile ProteinIntestineMyosinSerum Response FactorSmooth Muscle

Identifiers

PMID24151072
PMCPMC3843077
OpenAlexW2020005537

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.