Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Ca(2+) activation of myofilaments from transgenic mouse hearts expressing R92Q mutant cardiac troponin T.

American journal of physiology. Heart and circulatory physiology - 1 Feb 2001

Chandra M, Rundell V L, Tardiff J C, Leinwand L A, De Tombe P P, Solaro R J

Abstract excerpt

The functional consequences of the R92Q mutation in cardiac troponin T (cTnT), linked to familial hypertrophic cardiomyopathy in humans, are not well understood. We have studied steady- and pre-steady-state mechanical activity of detergent-skinned fiber bundles from a transgenic (TG) mouse model in which 67% of the total cTnT in the heart was replaced by the R92Q mutant cTnT. TG fibers were more sensitive to...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Genes, myc
Share to Acidosis

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Actin Cytoskeleton

Share to Cross-Linking Reagents

Share to Detergents

Share to Muscle Contraction

Share to Muscle Fibers, Skeletal

Share to Troponin T

Source

Identifiers

PMID: 11158969
DOI: 10.1152/ajpheart.2001.280.2.H705

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Ca(2+) activation of myofilaments from transgenic mouse hearts expressing R92Q mutant cardiac troponin T.PMID 11158969Read ↗

Cardiac troponin T mutations: correlation between the type of mutation and the nature of myofilament dysfunction in transgenic mice.Semantic proximity Read ↗

F110I and R278C troponin T mutations that cause familial hypertrophic cardiomyopathy affect muscle contraction in transgenic mice and reconstituted human cardiac fibers.Semantic proximity Read ↗

Investigation of a transgenic mouse model of familial dilated cardiomyopathy.Semantic proximity Read ↗

Temporal and mutation-specific alterations in Ca<sup>2+</sup> homeostasis differentially determine the progression of cTnT-related cardiomyopathies in murine modelsSemantic proximity Read ↗

The dilated cardiomyopathy-causing mutation ACTC E361G in cardiac muscle myofibrils specifically abolishes modulation of Ca(2+) regulation by phosphorylation of troponin I.Semantic proximity Read ↗

Abnormal contractile function in transgenic mice expressing a familial hypertrophic cardiomyopathy-linked troponin T (I79N) mutation.Semantic proximity Read ↗

Differential effect of troponin T mutations on the inotropic responsiveness of mouse hearts--role of myofilament Ca2+ sensitivity increase.Semantic proximity Read ↗

Independent FHC-related cardiac troponin T mutations exhibit specific alterations in myocellular contractility and calcium kinetics.Semantic proximity Read ↗

Alterations in thin filament regulation induced by a human cardiac troponin T mutant that causes dilated cardiomyopathy are distinct from those induced by troponin T mutants that cause hypertrophic cardiomyopathy.Semantic proximity Read ↗

Hypertrophic cardiomyopathy mutation in cardiac troponin T (R95H) attenuates length-dependent activation in guinea pig cardiac muscle fibers.Semantic proximity Read ↗

R-92L and R-92W mutations in cardiac troponin T lead to distinct energetic phenotypes in intact mouse hearts.Semantic proximity Read ↗

Protein kinase C and A sites on troponin I regulate myofilament Ca2+ sensitivity and ATPase activity in the mouse myocardium.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.