Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Localized phosphoinositide metabolism regulates STIM1/ORAI1 fast inactivation.

iScience·2026
Same author

REPLY: Is There an Intramyocardial "Purkinje" System in the Heart?

JACC. Clinical electrophysiology·2025
Same author

Healthspan-lifespan gap differs in magnitude and disease contribution across world regions.

Communications medicine·2025
Same author

MYL4 Identifies Intramural Anatomy of Purkinje Fibers in Human Hearts.

JACC. Clinical electrophysiology·2025
Same author

Myotubularin related protein 7, a novel STIM1 binding protein.

Canadian journal of physiology and pharmacology·2025
Same author

Maturation of human induced pluripotent stem cell-derived cardiomyocytes promoted by Brachyury priming.

Scientific reports·2025

Related Experiment Video

Updated: Apr 7, 2026

Combining Laser Capture Microdissection and Microfluidic qPCR to Analyze Transcriptional Profiles of Single Cells: A Systems Biology Approach to Opioid Dependence
09:54

Combining Laser Capture Microdissection and Microfluidic qPCR to Analyze Transcriptional Profiles of Single Cells: A Systems Biology Approach to Opioid Dependence

Published on: March 8, 2020

5.8K

Systems biology surveillance decrypts pathological transcriptome remodeling.

Randolph S Faustino1, Saranya P Wyles2, Jody Groenendyk3

  • 1Division of Cardiovascular Diseases, Departments of Medicine, Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA. Faustino.Randolph@mayo.edu.

BMC Systems Biology
|July 17, 2015
PubMed
Summary
This summary is machine-generated.

Calreticulin deficiency causes pathological cardiac development. This study used stem cell transcriptomes to identify gene networks underlying cardiac disease, revealing Pitx2 as a key regulator in calreticulin-compromised networks.

More Related Videos

Systems Biology of Metabolic Regulation by Estrogen Receptor Signaling in Breast Cancer
10:36

Systems Biology of Metabolic Regulation by Estrogen Receptor Signaling in Breast Cancer

Published on: March 17, 2016

11.0K
Purification of Transcripts and Metabolites from Drosophila Heads
12:49

Purification of Transcripts and Metabolites from Drosophila Heads

Published on: March 15, 2013

22.7K

Related Experiment Videos

Last Updated: Apr 7, 2026

Combining Laser Capture Microdissection and Microfluidic qPCR to Analyze Transcriptional Profiles of Single Cells: A Systems Biology Approach to Opioid Dependence
09:54

Combining Laser Capture Microdissection and Microfluidic qPCR to Analyze Transcriptional Profiles of Single Cells: A Systems Biology Approach to Opioid Dependence

Published on: March 8, 2020

5.8K
Systems Biology of Metabolic Regulation by Estrogen Receptor Signaling in Breast Cancer
10:36

Systems Biology of Metabolic Regulation by Estrogen Receptor Signaling in Breast Cancer

Published on: March 17, 2016

11.0K
Purification of Transcripts and Metabolites from Drosophila Heads
12:49

Purification of Transcripts and Metabolites from Drosophila Heads

Published on: March 15, 2013

22.7K

Area of Science:

  • Cardiovascular Biology
  • Stem Cell Biology
  • Molecular Genetics

Background:

  • Calreticulin (CALR) is an endoplasmic reticulum chaperone crucial for cardiogenesis.
  • CALR dysregulation leads to pathological cardiac development and embryonic lethality.
  • Understanding CALR's domain-specific functions is vital for deciphering cardiac formation pathways.

Purpose of the Study:

  • To investigate the molecular mechanisms of cardiac development affected by CALR deficiency.
  • To identify specific gene expression changes and regulatory networks influenced by CALR domains.
  • To decrypt the role of CALR in cardiopathology using pluripotent stem cells.

Main Methods:

  • Utilized wild type, CALR-deficient, and CALR truncation variant pluripotent stem cells.
  • Performed bioinformatic deconvolution of transcriptomes to identify expression trends and gene networks.
  • Employed unsupervised clustering and Kohonen mapping for RNA expression analysis.

Main Results:

  • CALR variants exhibited distinct molecular signatures.
  • Transcriptome analysis revealed 12 gene expression meta-profiles enriched for Eukaryotic Initiation Factor 2 (EIF2) signaling.
  • Cardiovascular Disease pathways were uniquely downregulated in the CALR-PC variant, highlighting Pitx2 as a critical network hub.

Conclusions:

  • An integrated algorithm of stem cell transcriptomes and bioinformatics can identify disease effectors.
  • Stem cell transcriptomes serve as a molecular index for gene network robustness.
  • This approach effectively decrypts gene expression changes in disrupted genomes for disease insight.