ArticleThe Journal of cell biology2002
Calreticulin reveals a critical Ca(2+) checkpoint in cardiac myofibrillogenesis.
Article in The Journal of cell biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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.
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.
Who cites it
30 citing papers in PubMed, 92 citations in OpenAlex.
- Human plasma-like medium enhances structural and metabolic maturation of human pluripotent stem cell-derived cardiomyocytes.Bioengineering & translational medicine · 2026Article
- Calreticulin and the Heart.Cells · 2022Review
- Stimulating Calcium Handling in hiPSC-Derived Engineered Cardiac Tissues Enhances Force Production.Stem cells translational medicine · 2022Article
- Novel dilated cardiomyopathy associated to Calreticulin and Myo7A gene mutation in Usher syndrome.ESC heart failure · 2021Article
- S-nitrosoglutathione reductase (GSNOR) deficiency accelerates cardiomyocyte differentiation of induced pluripotent stem cells.The journal of cardiovascular aging · 2021Article
- Selective enhancement of cardiomyocyte efficiency results in a pernicious heart condition.PloS one · 2020Article
- Mechanisms of protein homeostasis (proteostasis) maintain stem cell identity in mammalian pluripotent stem cells.Cellular and molecular life sciences : CMLS · 2018Review
- Article
- Nuclear Pores Regulate Muscle Development and Maintenance by Assembling a Localized Mef2C Complex.Developmental cell · 2017Article
- Defined Engineered Human Myocardium With Advanced Maturation for Applications in Heart Failure Modeling and Repair.Circulation · 2017Article
- Calreticulin Is Required for TGF-β-Induced Epithelial-to-Mesenchymal Transition during Cardiogenesis in Mouse Embryonic Stem Cells.Stem cell reports · 2017Article
- Somatic increase of CCT8 mimics proteostasis of human pluripotent stem cells and extends C. elegans lifespan.Nature communications · 2016Article
- Article
- Systems biology surveillance decrypts pathological transcriptome remodeling.BMC systems biology · 2015Article
- Molecular characterisation and expression analysis of a novel calreticulin (CRT) gene in the dinoflagellate Prorocentrum minimum.Molecular biology reports · 2015Article
- Disrupted WNT signaling in mouse embryonic stem cells in the absence of calreticulin.Stem cell reviews and reports · 2014Article
- Calreticulin induces dilated cardiomyopathy.PloS one · 2013Article
- A genome-wide siRNA screen identifies novel phospho-enzymes affecting Wnt/β-catenin signaling in mouse embryonic stem cells.Stem cell reviews and reports · 2011Article
- Organellar calcium buffers.Cold Spring Harbor perspectives in biology · 2011Review
- Decoded calreticulin-deficient embryonic stem cell transcriptome resolves latent cardiophenotype.Stem cells (Dayton, Ohio) · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calreticulin (crt) is an ubiquitously expressed and multifunctional Ca(2+)-binding protein that regulates diverse vital cell functions, including Ca(2+) storage in the ER and protein folding. Calreticulin deficiency in mice is lethal in utero due to defects in heart development and function. Herein, we used crt(-/-) embryonic stem (ES) cells differentiated in vitro into cardiac cells to investigate the molecular mechanisms underlying heart failure of knockout embryos. After 8 d of differentiation, beating areas were prominent in ES-derived wild-type (wt) embryoid bodies (EBs), but not in ES-derived crt(-/-) EBs, despite normal expression levels of cardiac transcription factors. Crt(-/-) EBs exhibited a severe decrease in expression and a lack of phosphorylation of ventricular myosin light chain 2 (MLC2v), resulting in an impaired organization of myofibrils. Crt(-/-) phenotype could be recreated in wt cells by chelating extracellular or cytoplasmic Ca(2+) with EGTA or BAPTA, or by inhibiting Ca(2+)/calmodulin-dependent kinases (CaMKs). An imposed ionomycin-triggered cystolic-free Ca(2+) concentration ([Ca(2+)](c)) elevation restored the expression, phosphorylation, and insertion of MLC2v into sarcomeric structures and in turn the myofibrillogenesis. The transcription factor myocyte enhancer factor C2 failed to accumulate into nuclei of crt(-/-) cardiac cells in the absence of ionomycin-triggered [Ca(2+)](c) increase. We conclude that the absence of calreticulin interferes with myofibril formation. Most importantly, calreticulin deficiency revealed the importance of a Ca(2+)-dependent checkpoint critical for early events during cardiac myofibrillogenesis.
Indexed as
Identifiers
What OpenQuestion holds
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.