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 Experiment Videos

Actin'g against the Ball and Chain.

Jasmine V G Abella1, Michael Way1

  • 1Cellular Signalling and Cytoskeletal Function Laboratory, The Francis Crick Institute, Lincoln's Inn Fields Laboratory, 44 Lincoln's Inn Fields, London WC2A 3LY, UK.

Developmental Cell
|April 6, 2016
PubMed
Summary

Spinocerebellar ataxia type 13, a rare neurodegenerative disease, involves Kv3.3 potassium channel mutations. New research reveals Arp2/3-dependent actin polymerization influences Kv3.3 channel activity and its interaction with Hax-1.

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

Inorganic phosphate rapidly switches the stability of Arp2/3-induced actin branches.

The Journal of cell biology·2026
Same author

'Why is publishing so expensive?

Journal of cell science·2026
Same author

Vinorelbine enhances the efficacy of oncolytic vaccinia virus in a preclinical model of ovarian high-grade serous carcinoma.

Molecular therapy. Oncology·2026
Same author

At the helm of JCS - Editors-in-Chief past, present… and future.

Journal of cell science·2025
Same author

Branched actin networks mediate macrophage-dependent host-microbiota homeostasis.

Science (New York, N.Y.)·2025
Same author

Arp2/3-mediated bidirectional actin assembly by SPIN90 dimers.

Nature structural & molecular biology·2025

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Spinocerebellar ataxia type 13 (SCA13) is a rare autosomal-dominant neurodegenerative disorder.
  • SCA13 is caused by mutations in the gene encoding the voltage-dependent Kv3.3 potassium channel.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying SCA13.
  • To explore the relationship between Kv3.3 potassium channel function and actin dynamics.

Main Methods:

  • Utilized molecular biology techniques to study Kv3.3 channel function.
  • Investigated the role of Arp2/3 complex and Hax-1 in modulating Kv3.3 activity.

Main Results:

  • Demonstrated that Arp2/3-dependent actin polymerization influences Kv3.3 channel activity.

Related Experiment Videos

  • Showed that Kv3.3 channels can stimulate actin polymerization through Hax-1.

    • Conclusions:

    • Actin polymerization is a key regulator of Kv3.3 channel function in the context of SCA13.
    • Findings provide new insights into the pathogenesis of SCA13 and potential therapeutic targets.