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Related Concept Videos

Feedback Regulation of Calcium Concentration01:27

Feedback Regulation of Calcium Concentration

Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...
Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
Smooth Muscle Contraction01:25

Smooth Muscle Contraction

Smooth muscle contraction is a complex process vital for various bodily functions, from maintaining blood vessel tension to facilitating the movement of food through the digestive tract. Unlike striated muscles, smooth muscle contraction begins more slowly and lasts longer.
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Positive Regulator Molecules01:45

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
Positive Regulator Molecules02:39

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.

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Related Experiment Video

Updated: Jun 26, 2026

Real-Time Measurements of Calcium and Contractility Parameters in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes
06:42

Real-Time Measurements of Calcium and Contractility Parameters in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes

Published on: May 26, 2023

Sequential changes in calcium transients during M phase regulate cardiomyocyte proliferation.

Honghai Liu1, Niyatie Ammanamanchi1, Jocelyn D Mich-Basso2,3

  • 1Department of Pediatrics, Weill Cornell Medical College, Cornell University, New York City, NY, USA.

The Journal of Cell Biology
|June 25, 2026
PubMed
Summary
This summary is machine-generated.

Cardiomyocyte proliferation involves dynamic changes in calcium transients (CaTs). Reduced Ca2+ at spindle poles, regulated by CDK1 and SERCA2a, is crucial for proper cell division and heart muscle regeneration.

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Visualization of Cell Cycle Variations and Determination of Nucleation in Postnatal Cardiomyocytes
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High-Throughput Optical Controlling and Recording Calcium Signal in iPSC-Derived Cardiomyocytes for Toxicity Testing and Phenotypic Drug Screening
10:01

High-Throughput Optical Controlling and Recording Calcium Signal in iPSC-Derived Cardiomyocytes for Toxicity Testing and Phenotypic Drug Screening

Published on: March 31, 2022

Related Experiment Videos

Last Updated: Jun 26, 2026

Real-Time Measurements of Calcium and Contractility Parameters in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes
06:42

Real-Time Measurements of Calcium and Contractility Parameters in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes

Published on: May 26, 2023

Visualization of Cell Cycle Variations and Determination of Nucleation in Postnatal Cardiomyocytes
09:41

Visualization of Cell Cycle Variations and Determination of Nucleation in Postnatal Cardiomyocytes

Published on: February 24, 2017

High-Throughput Optical Controlling and Recording Calcium Signal in iPSC-Derived Cardiomyocytes for Toxicity Testing and Phenotypic Drug Screening
10:01

High-Throughput Optical Controlling and Recording Calcium Signal in iPSC-Derived Cardiomyocytes for Toxicity Testing and Phenotypic Drug Screening

Published on: March 31, 2022

Area of Science:

  • Cardiovascular Biology
  • Cellular Signaling
  • Molecular Cardiology

Background:

  • Cardiomyocyte proliferation is essential for heart muscle growth and repair.
  • Calcium transients (CaTs) regulate cardiomyocyte contraction but their role in proliferation is unclear.

Purpose of the Study:

  • To investigate how calcium signaling adapts during cardiomyocyte proliferation.
  • To elucidate the mechanisms controlling Ca2+ dynamics in dividing cardiomyocytes.

Main Methods:

  • Monitoring CaT dynamics and Ca2+ levels at spindle poles during cardiomyocyte M phase.
  • Investigating the roles of cyclin-dependent kinase 1 (CDK1) and SERCA2a in Ca2+ regulation.
  • Utilizing pharmacological inhibition of SERCA2a to assess mitotic disruption.

Main Results:

  • Cardiomyocytes exhibit a specific sequence of CaT amplitude changes during M phase.
  • Ca2+ levels decrease at spindle poles during prometaphase and metaphase, mediated by dynein 1-dependent SERCA2a.
  • Active CDK1 drives both reduced CaT amplitudes and SERCA2a accumulation; CDK1 inhibition reverses these effects.
  • Blocking SERCA2a disrupts mitosis, leading to binucleated cardiomyocytes.

Conclusions:

  • Changes in Ca2+ signaling are integral to cardiomyocyte proliferation.
  • CDK1-mediated regulation of SERCA2a at spindle poles is critical for successful mitosis.
  • Precise control of cytosolic Ca2+ levels is essential for heart muscle cell division and regeneration.