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

GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

6.9K
Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
6.9K
Epistasis Analysis01:09

Epistasis Analysis

4.9K
Although Mendel chose seven unrelated traits in peas to study gene segregation, most traits involve multiple gene interactions that create a spectrum of phenotypes. When the interaction of various genes or alleles at different locations influences a phenotype, this is called epistasis. Epistasis often involves one gene masking or interfering with the expression of another (antagonistic epistasis). Epistasis often occurs when different genes are part of the same biochemical pathway. The...
4.9K
GPCR Desensitization01:12

GPCR Desensitization

6.2K
G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
6.2K

You might also read

Related Articles

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

Sort by
Same author

Photochemistry of CryB from Rhodobacter sphaeroides.

Photochemistry and photobiology·2026
Same author

Optically detected and radio wave-controlled spin chemistry in flavoproteins.

Nature biotechnology·2026
Same author

Biological and physiological properties of 7-ketocholesterol and interest in diseases and food industry.

The Journal of steroid biochemistry and molecular biology·2026
Same author

7-ketocholesterol as a theranostic target: Potential applications and future perspectives.

Chemistry and physics of lipids·2026
Same author

Pretreatment blood NfL indicates response to cellular therapies in cerebral adrenoleukodystrophy.

Communications medicine·2026
Same author

Synergistic Anticancer Activity of <i>Annona muricata</i> Leaf Extract and Cisplatin in 4T1 Triple-Negative Breast Cancer Cells.

Cells·2026

Related Experiment Video

Updated: May 5, 2026

Reverse Yeast Two-hybrid System to Identify Mammalian Nuclear Receptor Residues that Interact with Ligands and/or Antagonists
10:51

Reverse Yeast Two-hybrid System to Identify Mammalian Nuclear Receptor Residues that Interact with Ligands and/or Antagonists

Published on: November 15, 2013

11.9K

LXR antagonists induce ABCD2 expression.

Catherine Gondcaille, Emmanuelle C Genin, Tatiana E Lopez

    Biochimica Et Biophysica Acta
    |November 19, 2013
    PubMed
    Summary

    LXR antagonists up-regulate ABCD2 and ABCD3 genes, potentially treating X-linked adrenoleukodystrophy (X-ALD) by reducing oxidative stress. This offers a new therapeutic avenue for X-ALD patients.

    More Related Videos

    A Rapid In Vivo Bioassay for Developmentally Active Enhancers
    00:08

    A Rapid In Vivo Bioassay for Developmentally Active Enhancers

    1.2K
    In Vivo Augmentation of Gut-Homing Regulatory T Cell Induction
    08:02

    In Vivo Augmentation of Gut-Homing Regulatory T Cell Induction

    Published on: January 22, 2020

    4.9K

    Related Experiment Videos

    Last Updated: May 5, 2026

    Reverse Yeast Two-hybrid System to Identify Mammalian Nuclear Receptor Residues that Interact with Ligands and/or Antagonists
    10:51

    Reverse Yeast Two-hybrid System to Identify Mammalian Nuclear Receptor Residues that Interact with Ligands and/or Antagonists

    Published on: November 15, 2013

    11.9K
    A Rapid In Vivo Bioassay for Developmentally Active Enhancers
    00:08

    A Rapid In Vivo Bioassay for Developmentally Active Enhancers

    1.2K
    In Vivo Augmentation of Gut-Homing Regulatory T Cell Induction
    08:02

    In Vivo Augmentation of Gut-Homing Regulatory T Cell Induction

    Published on: January 22, 2020

    4.9K

    Area of Science:

    • Biochemistry
    • Genetics
    • Neuroscience

    Background:

    • X-linked adrenoleukodystrophy (X-ALD) is a neurodegenerative disorder caused by ABCDI gene mutations, leading to very-long-chain fatty acid accumulation.
    • Oxidative stress and inflammation are key pathological features of X-ALD.
    • ABCD2 and ABCD3 transporters can compensate for ABCD1 deficiency, suggesting therapeutic potential through their induction.

    Purpose of the Study:

    • To investigate the effect of Liver X Receptor (LXR) antagonists on ABCD2 and ABCD3 gene expression.
    • To explore LXR antagonists as a potential therapeutic strategy for X-ALD.

    Main Methods:

    • Treatment of human HepG2 cells and X-ALD skin fibroblasts with LXR antagonists (GSK'17, 22S-HC).
    • Analysis of ABCD2, ABCD3, and CTNNB1 gene expression.
    • Assessment of oxidative stress markers in X-ALD fibroblasts.
    • In vivo studies in rats and human tissue expression analysis.

    Main Results:

    • LXR antagonists significantly up-regulated ABCD2, ABCD3, and CTNNB1 genes in cell lines.
    • X-ALD fibroblasts showed decreased oxidative stress upon treatment.
    • Hepatic induction of target genes was observed in rats treated with 22S-HC.
    • Human ABCD2 expression inversely correlated with NR1H3 (LXRalpha) expression.

    Conclusions:

    • LXR antagonists show promise for X-ALD therapy by inducing compensatory ABCD genes.
    • Targeting LXR represents a novel therapeutic strategy for X-ALD, potentially repurposing dyslipidemia drugs.