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

Gene Knock-Outs of Inositol 1,4,5-Trisphosphate Receptors Types 1 and 2 Result in Perturbation of Cardiogenesis

1 Sept 2010

Abstract excerpt

BACKGROUND: Inositol 1,4,5-trisphosphate receptors (IP3R1, 2, and 3) are intracellular Ca2+ release channels that regulate various vital processes. Although the ryanodine receptor type 2, another type of intracellular Ca2+ release channel, has been shown to play a role in embryonic cardiomyocytes, the functions of the IP3Rs in cardiogenesis remain unclear. METHODOLOGY/PRINCIPAL FINDINGS: We found that...

Read the complete abstract on PubMed

Topics

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

Share to Calcium signaling and nucleotide metabolism
Share to Cardiac electrophysiology and arrhythmias
Share to Signaling Pathways in Disease

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

Source

Identifiers

PMID: 20824138
DOI: 10.1371/journal.pone.0012500

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 23 Oct 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

Gene Knock-Outs of Inositol 1,4,5-Trisphosphate Receptors Types 1 and 2 Result in Perturbation of CardiogenesisPMID 20824138Read ↗

NFATc3 and NFATc4 are required for cardiac development and mitochondrial function.Semantic proximity Read ↗

Heart-specific Deletion of CnB1 Reveals Multiple Mechanisms Whereby Calcineurin Regulates Cardiac Growth and FunctionSemantic proximity Read ↗

Cardiac-specific Expression of Calcineurin Reverses Embryonic Lethality in Calreticulin-deficient MouseSemantic proximity Read ↗

Inositol 1,4,5-trisphosphate-mediated sarcoplasmic reticulum-mitochondrial crosstalk influences adenosine triphosphate production via mitochondrial Ca2+ uptake through the mitochondrial ryanodine receptor in cardiac myocytes.Semantic proximity Read ↗

Pathophysiological Significance of T-type Ca2+ Channels: Expression of T-type Ca2+ Channels in Fetal and Diseased HeartSemantic proximity Read ↗

Functionally redundant control of cardiac hypertrophic signaling by inositol 1,4,5-trisphosphate receptorsSemantic proximity Read ↗

CaV3.2 T-type channels mediate Ca2+ entry during oocyte maturation and following fertilizationSemantic proximity Read ↗

Type 1 inositol 1,4,5-trisphosphate receptor knock-out mice: their phenotypes and their meaning in neuroscience and clinical practice.Semantic proximity Read ↗

Calreticulin signals upstream of calcineurin and MEF2C in a critical Ca2+-dependent signaling cascadeSemantic proximity Read ↗

Disruption of the mouse inositol 1,3,4,5,6-pentakisphosphate 2-kinase gene, associated lethality, and tissue distribution of 2-kinase expression.Semantic proximity Read ↗

Embryonic Lethality in Mice Lacking the Nuclear Factor of Activated T Cells 5 Protein Due to Impaired Cardiac Development and FunctionSemantic proximity Read ↗

The IP3 receptor regulates cardiac hypertrophy in response to select stimuli.Semantic proximity Read ↗

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