ArticleThe Journal of clinical investigation2001
Complete heart block and sudden death in mice overexpressing calreticulin.
Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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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.
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Who cites it
48 citing papers in PubMed, 138 citations in OpenAlex.
- Reduction of calreticulin and ERp57 with age reveals the ER stress-related roles in cell viability and organismal lifespan regulation.Frontiers in aging · 2026Article
- A highly effective, rodent model of complete heart block by epicardial radiofrequency ablation.Scientific reports · 2025Article
- Calreticulin-From the Endoplasmic Reticulum to the Plasma Membrane-Adventures of a Wandering Protein.Cancers · 2025Review
- What to consider for ECG in mice-with special emphasis on telemetry.Mammalian genome : official journal of the International Mammalian Genome Society · 2023Review
- Calreticulin and the Heart.Cells · 2022Review
- The ATF6β-calreticulin axis promotes neuronal survival under endoplasmic reticulum stress and excitotoxicity.Scientific reports · 2021Article
- TET2, DNMT3A, IDH1, and JAK2 Mutation in Myeloproliferative Neoplasms in southern Iran.International journal of organ transplantation medicine · 2021Article
- Calreticulin and cancer.Cell research · 2021Review
- Calreticulin expression in human cardiac myocytes induces ER stress-associated apoptosis.Physiological reports · 2020Article
- A rat model of complete atrioventricular block recapitulates clinical indices of bradycardia and provides a platform to test disease-modifying therapies.Scientific reports · 2019Article
- Lack of evidence for a causal role of CALR3 in monogenic cardiomyopathy.European journal of human genetics : EJHG · 2018Article
- CaThe Journal of physiology · 2017Review
- Calreticulin Is Required for TGF-β-Induced Epithelial-to-Mesenchymal Transition during Cardiogenesis in Mouse Embryonic Stem Cells.Stem cell reports · 2017Article
- The Mutation Profile of Calreticulin in Patients with Myeloproliferative Neoplasms and Acute Leukemia.Turkish journal of haematology : official journal of Turkish Society of Haematology · 2016Article
- Coexistence of JAK2 and CALR mutations and their clinical implications in patients with essential thrombocythemia.Oncotarget · 2016Article
- Genetic variations involved in sudden cardiac death and their associations and interactions.Heart failure reviews · 2016Review
- Systems biology surveillance decrypts pathological transcriptome remodeling.BMC systems biology · 2015Article
- Calreticulin is localized at mitochondria of rat cardiomyocytes and affected by furazolidone.Molecular and cellular biochemistry · 2014Article
- CALR vs JAK2 vs MPL-mutated or triple-negative myelofibrosis: clinical, cytogenetic and molecular comparisons.Leukemia · 2014Article
- Calreticulin negatively regulates the surface expression of Cav1.3 L-type calcium channel.Biochemical and biophysical research communications · 2013Article
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The expression of calreticulin, a Ca(2+)-binding chaperone of the endoplasmic reticulum, is elevated in the embryonic heart, and because of impaired cardiac development, knockout of the Calreticulin gene is lethal during embryogenesis. The elevated expression is downregulated after birth. Here we have investigated the physiological consequences of continued high expression of calreticulin in the postnatal heart, by producing transgenic mice that overexpress the protein in the heart. These transgenic animals exhibit decreased systolic function and inward I(Ca,L), low levels of connexin43 and connexin40, sinus bradycardia, and prolonged atrioventricular (AV) node conduction followed by complete heart block and sudden death. We conclude that postnatal downregulation of calreticulin is essential in the development of the cardiac conductive system, in particular in the sinus and AV nodes, when an inward Ca(2+) current is required for activation. This work identifies a novel pathway of events, leading to complete heart block and sudden cardiac death, which involves high expression of calreticulin in the heart.
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Registered trials
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.