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Related Concept Videos

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.
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Related Experiment Video

Updated: Jun 3, 2026

Measuring Intracellular Ca2+ Changes in Human Sperm using Four Techniques: Conventional Fluorometry, Stopped Flow Fluorometry, Flow Cytometry and Single Cell Imaging
19:26

Measuring Intracellular Ca2+ Changes in Human Sperm using Four Techniques: Conventional Fluorometry, Stopped Flow Fluorometry, Flow Cytometry and Single Cell Imaging

Published on: May 24, 2013

Two distinct Ca(2+) signaling pathways modulate sperm flagellar beating patterns in mice.

Haixin Chang1, Susan S Suarez

  • 1Department of Biomedical Sciences, Cornell University, Ithaca, NY 14853, USA.

Biology of Reproduction
|March 11, 2011
PubMed
Summary

Sperm hyperactivation, crucial for fertilization, involves Ca(2+) signaling that dictates flagellar bend direction. Different Ca(2+) pathways control pro-hook and anti-hook bends, potentially redirecting sperm towards oocytes.

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Last Updated: Jun 3, 2026

Measuring Intracellular Ca2+ Changes in Human Sperm using Four Techniques: Conventional Fluorometry, Stopped Flow Fluorometry, Flow Cytometry and Single Cell Imaging
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Measuring Sperm Guidance and Motility within the Caenorhabditis elegans Hermaphrodite Reproductive Tract

Published on: June 6, 2019

Area of Science:

  • Reproductive Biology
  • Cellular Physiology
  • Sperm Motility

Background:

  • Sperm hyperactivation is a critical Ca(2+)-dependent swimming pattern for mammalian fertilization.
  • This pattern involves asymmetrical flagellar beating and distinct bend formations (pro-hook and anti-hook).
  • Understanding the Ca(2+) signaling pathways governing these bends is key to deciphering sperm navigation.

Purpose of the Study:

  • To investigate the distinct Ca(2+) signaling pathways responsible for high-amplitude pro-hook and anti-hook bends during sperm hyperactivation.
  • To determine how these pathways influence sperm redirection towards oocytes.

Main Methods:

  • In vitro analysis of mouse sperm capacitation and hyperactivation.
  • Treatment with CATSPER channel activators (procaine, 4-aminopyridine) and intracellular Ca(2+) releaser (thimerosal).
  • Monitoring of intracellular Ca(2+) and flagellar pH changes; examination of protein phosphorylation patterns.

Main Results:

  • CATSPER activation (procaine, 4-AP) induced high-amplitude pro-hook bends and serine/threonine protein phosphorylation.
  • Thimerosal triggered high-amplitude anti-hook bends via intracellular Ca(2+) release, causing protein dephosphorylation.
  • 4-AP induced a flagellar pH rise, while thimerosal did not.

Conclusions:

  • Sperm hyperactivation's bend direction can be modulated by intracellular Ca(2+) release.
  • Distinct Ca(2+) signaling pathways differentially regulate flagellar bending and protein phosphorylation.
  • This modulation offers a mechanism for redirecting sperm during fertilization.