Evidence map›Paper›PMID 23727233›Full record

ArticleJournal of molecular and cellular cardiology2013

Diversity and similarity of motor function and cross-bridge kinetics in papillary muscles of transgenic mice carrying myosin regulatory light chain mutations D166V and R58Q.

Li Wang, Priya Muthu, Danuta Szczesna-Cordary, Masataka Kawai

Abstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 20 citations in OpenAlex.

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  7. Slow-twitch skeletal muscle defects accompany cardiac dysfunction in transgenic mice with a mutation in the myosin regulatory light chain.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
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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

4 authors at 2 institutions in 1 country.

Li WangDepartment of Anatomy and Cell Biology, University of Iowa, Iowa City, IA 52242, USA. li-wang-1@uiowa.edu
Priya Muthu
Danuta Szczesna-Cordary
Masataka Kawai
University of Iowa · USUniversity of Miami · US

Funding

Functional Consequences of FHC-linked RLC Mutations.R01HL071778 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SZCZESNA-CORDARY, DANUTA · 2003 to 2012
$3.5M
Role of actin domains in force generation in myocardiumR01HL070041 · NHLBI · UNIVERSITY OF IOWA · PI KAWAI, MASATAKA · 2002 to 2011
$2.5M
Single Cross-Bridge Kinetics in Transgenic Mouse Hearts Expressing FHC MutationsR01HL090786 · NHLBI · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI BOREJDO, JULIAN, SZCZESNA-CORDARY, DANUTA · 2009 to 2012
$1.6M
Myosin ELC, a novel therapeutic target for FHCR01HL108343 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SZCZESNA-CORDARY, DANUTA · 2012 to 2015
$1.5M
NHLBI NIH HHS HL070041NHLBI NIH HHS HL071778NHLBI NIH HHS HL090786NHLBI NIH HHS HL108343NHLBI NIH HHS R01 HL070041NHLBI NIH HHS R01 HL071778NHLBI NIH HHS R01 HL090786NHLBI NIH HHS R01 HL108343
6 · The paper itself

Abstract

Mechanical properties of skinned papillary muscle fibers from transgenic mice expressing familial hypertrophic cardiomyopathy associated mutations D166V and R58Q in myosin regulatory light chain were investigated. Elementary steps and the apparent rate constants of the cross-bridge cycle were characterized from the tension transients induced by sinusoidal length changes during maximal Ca(2+) activation, together with ATP, ADP, and Pi studies. The tension-pCa relation was also tested in two sets of solutions with differing Pi and ionic strength. Our results showed that in both mutants the fast apparent rate constant 2πc and the rate constants of the cross-bridge detachment step (k2) were smaller than those of wild type (WT), demonstrating the slower cross-bridge kinetics. D166V showed significantly smaller ATP (K1) and ADP (K0) association constants than WT, displaying weaker ATP binding and easier ADP release, whereas those of R58Q were not significantly different from WT. In tension-pCa study, both D166V and R58Q mutations exhibited increased Ca(2+) sensitivity and less cooperativity. We conclude that, while the two FHC mutations have similar clinical manifestations and prognosis, some of the mechanical parameters of cross-bridges (K0, K1) are differently modified, whereas some others (Ca(2+)-sensitivity, cooperativity, k2) are similarly modified by these two FHC associated mutations.

Indexed as

Adenosine TriphosphateAnimalsCalciumCardiomyopathiesHumansMiceMice, TransgenicModels, TheoreticalMutationMyosin Light ChainsPapillary MusclesProtein BindingAdenosine TriphosphateCalciumMyosin Light ChainsCardiac contractilityCardiomyopathyElementary stepsMyosin regulatory light chainSinusoidal analysis

Identifiers

PMID23727233
PMCPMC3809071
OpenAlexW1992935663

What OpenQuestion holds

Textmetadata
LicenceTDM
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.