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

Blast exposure causes dynamic microglial/macrophage responses and microdomains of brain microvessel dysfunction.

Neuroscience·2016
Same author

Reduced activity of AMP-activated protein kinase protects against genetic models of motor neuron disease.

The Journal of neuroscience : the official journal of the Society for Neuroscience·2012
Same author

The influence of cadence and power output on force application and in-shoe pressure distribution during cycling by competitive and recreational cyclists.

Journal of sports sciences·2000
Same author

Effects of three-dimensional assessment on surgical correction and on hook strategies in multi-hook instrumentation for adolescent idiopathic scoliosis.

Spine·1998
Same author

Operant conditioning and discrimination of alpha: some methodological limitations inherent in response-discrimination experiments.

Journal of experimental psychology. General·1981
Same author

Effects of fornix lesions on adrenocortical responses to changes in environmental stimulation.

Behavioral and neural biology·1979
Same journal

Utrophin requires α-Syntrophin to maintain neuromuscular junction integrity in mdx mice.

Human molecular genetics·2026
Same journal

A novel gene ACTRT3 mutations induce sperm malformations and fertilization failure via Acrosomal ultrastructural defects.

Human molecular genetics·2026
Same journal

Nucleic acid-based therapeutic strategies for modulator-refractory cystic fibrosis-causing variants.

Human molecular genetics·2026
Same journal

Evidence that disruption of Discoidin domain receptor 2 contributes to palate malformations through effects on the extracellular matrix.

Human molecular genetics·2026
Same journal

Nicotinamide riboside prevents mitochondrial dysfunction in nemaline myopathy type 6.

Human molecular genetics·2026
Same journal

Retraction: Aqua-soluble DDQ reduces the levels of Dr1 and Ab and inhibits abnormal interactions between Ab and Dr1 and protects Alzheimer's disease neurons from Ab- and Dr1-induced mitochondrial and synaptic toxicities.

Human molecular genetics·2026
See all related articles

Related Experiment Video

Updated: Aug 4, 2025

Author Spotlight: Understanding the Impact of Pathological Proteins on Axonal Transport in Neurodegenerative Diseases
10:38

Author Spotlight: Understanding the Impact of Pathological Proteins on Axonal Transport in Neurodegenerative Diseases

Published on: December 22, 2023

563

Sut-6/NIPP1 modulates tau toxicity.

R L Kow1,2, A H Black1, B P Henderson1

  • 1Geriatrics Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA 98108, USA.

Human Molecular Genetics
|March 31, 2023
PubMed
Summary
This summary is machine-generated.

Researchers identified a new gene, sut-6 (homologous to human NIPP1), that suppresses tauopathy. A specific mutation in sut-6 strongly reduces tau toxicity, offering potential therapeutic strategies for neurodegenerative diseases like Alzheimer's.

More Related Videos

Modulation of Tau Subcellular Localization as a Tool to Investigate the Expression of Disease-related Genes
09:12

Modulation of Tau Subcellular Localization as a Tool to Investigate the Expression of Disease-related Genes

Published on: December 20, 2019

6.4K
An In Vitro Model for Studying Tau Aggregation Using Lentiviral-mediated Transduction of Human Neurons
05:51

An In Vitro Model for Studying Tau Aggregation Using Lentiviral-mediated Transduction of Human Neurons

Published on: May 23, 2019

6.0K

Related Experiment Videos

Last Updated: Aug 4, 2025

Author Spotlight: Understanding the Impact of Pathological Proteins on Axonal Transport in Neurodegenerative Diseases
10:38

Author Spotlight: Understanding the Impact of Pathological Proteins on Axonal Transport in Neurodegenerative Diseases

Published on: December 22, 2023

563
Modulation of Tau Subcellular Localization as a Tool to Investigate the Expression of Disease-related Genes
09:12

Modulation of Tau Subcellular Localization as a Tool to Investigate the Expression of Disease-related Genes

Published on: December 20, 2019

6.4K
An In Vitro Model for Studying Tau Aggregation Using Lentiviral-mediated Transduction of Human Neurons
05:51

An In Vitro Model for Studying Tau Aggregation Using Lentiviral-mediated Transduction of Human Neurons

Published on: May 23, 2019

6.0K

Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Neurodegenerative diseases like Alzheimer's are characterized by tau pathology and lack effective treatments.
  • Understanding the molecular mechanisms of neurodegeneration and identifying tau toxicity modulators is crucial.

Purpose of the Study:

  • To discover novel suppressor of tauopathy (sut) genes.
  • To investigate the role of C. elegans sut-6, the homolog of human NIPP1, in modulating tau toxicity.

Main Methods:

  • Classical genetic screening in a tau transgenic Caenorhabditis elegans model.
  • CRISPR-based genome editing to generate sut-6 null and truncated alleles.
  • Epistasis studies to determine genetic interactions.

Main Results:

  • A mutation (W292X) in sut-6, truncating its RNA-binding domain, was identified as a potent suppressor of tau toxicity.
  • Loss of sut-6 or the W292X mutation suppressed tau-induced behavioral deficits, tau accumulation, and neuron loss.
  • The W292X mutation exhibited semi-dominant suppression, while sut-6 deletion was recessive.
  • Neuronal overexpression of the SUT-6 W292X mutant protein reduced tau-mediated deficits, unlike wild-type SUT-6.

Conclusions:

  • sut-6/NIPP1 plays a significant role in modulating tau toxicity.
  • A dominant mutation in the sut-6 RNA-binding domain strongly suppresses tauopathy.
  • Targeting RNA-related functions of SUT-6/NIPP1 may offer a more effective therapeutic strategy than complete loss of function.