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

RNA Splicing01:32

RNA Splicing

60.8K
Splicing is the process by which eukaryotic RNA is edited before its translation into protein. The RNA strand transcribed from eukaryotic DNA is called the primary transcript. The primary transcripts that become mRNAs are called precursor messenger RNAs (pre-mRNAs). Eukaryotic pre-mRNA contains alternating sequences of exons and introns. Exons are nucleotide sequences that code for proteins, whereas introns are the non-coding regions. In RNA splicing, introns are removed and exons are bonded...
60.8K
Alternative RNA Splicing02:18

Alternative RNA Splicing

25.3K
Alternative RNA splicing is the regulated splicing of exons and introns to produce different mature mRNAs from a single pre-mRNA. Unlike in constitutive splicing where a single gene produces a single type of mRNA, alternative splicing allows an organism to produce multiple proteins from a single gene and plays an important role in protein diversity.
There are five types of alternative RNA splicing that vary in the ways the pre-mRNA segments are removed or retained in the mature mRNA. The first...
25.3K
RNA Editing02:23

RNA Editing

9.9K
RNA editing is a post-transcriptional modification where a precursor mRNA (pre-mRNA) nucleotide sequence is changed by base insertion, deletion, or modification. The extent of RNA editing varies from a few hundred bases, in mitochondrial DNA of trypanosomes, to a just single base, in nuclear genes of mammals. Even a single base change in the pre-mRNA can convert a codon for one amino acid into the codon for another amino acid or a stop codon. This type of re-coding can significantly affect the...
9.9K
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

1.8K
Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
1.8K
Nonsense-mediated mRNA Decay02:27

Nonsense-mediated mRNA Decay

12.0K
The Upf proteins that carry out nonsense-mediated decay (NMD) are found in all eukaryotic organisms, including humans. Each protein has an individual role, but they need to work in collaboration. Upf1 is an ATP-dependent RNA helicase that unwinds the RNA helix. Because Upf1 can unwind any RNA, Upf2 and Upf3 are required to help Upf1 discriminate between nonsense and normal mRNAs.
Usually, Upf3 binds to an Exon Junction Complex (EJC) at mRNA splice sites. If a ribosome fully translates the mRNA,...
12.0K
Nonsense-mediated mRNA Decay02:27

Nonsense-mediated mRNA Decay

3.5K
3.5K

You might also read

Related Articles

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

Sort by
Same author

Investigating Alzheimer's Disease-Associated Genes Using Differential Splicing Frequency Analysis.

Cells·2026
Same author

Emergence of crucial evidence catalyzing the origin tracing of SARS-CoV-2.

PloS one·2024
Same author

Re-analysis of single-cell RNA-seq data reveals the origin and roles of cycling myeloid cells.

Stem cells (Dayton, Ohio)·2024
Same author

PacBio full-length transcriptome analysis provides new insights into transcription of chloroplast genomes.

RNA biology·2023
Same author

Full-length genome sequence of segmented RNA virus from ticks was obtained using small RNA sequencing data.

BMC genomics·2020
Same author

Precise annotation of tick mitochondrial genomes reveals multiple copy number variation of short tandem repeats and one transposon-like element.

BMC genomics·2020
Same journal

Novel Variants in PLPBP, SCN1A, and SLC6A1: Genetics, Bioinformatics, and clinical Elucidation of Three Distinct Cases of Developmental and Epileptic Encephalopathy.

Journal of neurogenetics·2026
Same journal

D-ribose-L-cysteine protects against rotenone-induced neurotoxicity in <i>Drosophila</i> via redox, neurotransmitter, and DDC gene regulation.

Journal of neurogenetics·2026
Same journal

Genetic architecture of hereditary spastic paraplegia: from monogenic to oligogenic models.

Journal of neurogenetics·2026
Same journal

Expression of sulfate pathway genes in human neurodevelopment.

Journal of neurogenetics·2026
Same journal

<i>Nckx30c</i>, a <i>Drosophila</i> K<sup>+</sup>-dependent Na<sup>+</sup>/Ca<sup>2+</sup> exchanger, regulates temperature-sensitive convulsions and age-related neurodegeneration.

Journal of neurogenetics·2026
Same journal

A zinc finger MYM-type containing 3 (ZMYM3) allele is associated with autism spectrum disorder in Iranian people.

Journal of neurogenetics·2026
See all related articles

Related Experiment Video

Updated: Feb 19, 2026

A Reporter Based Cellular Assay for Monitoring Splicing Efficiency
08:53

A Reporter Based Cellular Assay for Monitoring Splicing Efficiency

Published on: September 15, 2021

3.3K

Overexpression of U1 snRNA induces decrease of U1 spliceosome function associated with Alzheimer's disease.

Zhi Cheng1, Yingchun Shang1, Shan Gao1

  • 1a College of Life Sciences and Key Laboratory of Bioactive Materials Ministry of Education , Nankai University , Tianjin , PR China.

Journal of Neurogenetics
|November 4, 2017
PubMed
Summary
This summary is machine-generated.

Altering U1 small nuclear RNA (snRNA) function disrupts cellular processes, impacting Alzheimer's disease (AD) gene expression, tau pathology, and cell viability, suggesting U1 snRNA as a potential therapeutic target.

Keywords:
Alzheimer’s diseaseAβThr212U1 snRNAfunctional knockdownnecroptosis

More Related Videos

ACT1-CUP1 Assays Determine the Substrate-Specific Sensitivities of Spliceosomal Mutants in Budding Yeast
07:31

ACT1-CUP1 Assays Determine the Substrate-Specific Sensitivities of Spliceosomal Mutants in Budding Yeast

Published on: June 30, 2022

3.0K
Analysis of Spliceosomal snRNA Localization in Human Hela Cells Using Microinjection
07:35

Analysis of Spliceosomal snRNA Localization in Human Hela Cells Using Microinjection

Published on: August 6, 2019

6.5K

Related Experiment Videos

Last Updated: Feb 19, 2026

A Reporter Based Cellular Assay for Monitoring Splicing Efficiency
08:53

A Reporter Based Cellular Assay for Monitoring Splicing Efficiency

Published on: September 15, 2021

3.3K
ACT1-CUP1 Assays Determine the Substrate-Specific Sensitivities of Spliceosomal Mutants in Budding Yeast
07:31

ACT1-CUP1 Assays Determine the Substrate-Specific Sensitivities of Spliceosomal Mutants in Budding Yeast

Published on: June 30, 2022

3.0K
Analysis of Spliceosomal snRNA Localization in Human Hela Cells Using Microinjection
07:35

Analysis of Spliceosomal snRNA Localization in Human Hela Cells Using Microinjection

Published on: August 6, 2019

6.5K

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Presenilin-1 (PS1) influences amyloid precursor protein (APP) expression, beta-amyloid levels, and cell death.
  • U1 small nuclear RNA (snRNA) expression is linked to these changes.

Purpose of the Study:

  • To investigate the functional consequences of altering U1 snRNA levels on Alzheimer's disease (AD) relevant pathways.
  • To explore U1 snRNA's role in neurodegeneration and identify potential therapeutic targets.

Main Methods:

  • Manipulating U1 snRNA expression (overexpression and knockdown) in cellular models.
  • Analyzing downstream effects on gene expression, protein modifications, and cell viability.

Main Results:

  • Both U1 snRNA overexpression and knockdown impaired U1 snRNA function, leading to PCPA.
  • Observed AD-specific gene expression changes, tau hyperphosphorylation at Thr212, decreased acetylated α-tubulin, reduced cell viability, and increased RIPK1, RIPK3, and caspase-8.
  • These effects mirror those seen with PS1 induction.

Conclusions:

  • U1 snRNA plays a critical role in cellular homeostasis and AD pathogenesis.
  • Dysregulation of U1 snRNA contributes to key pathological features of Alzheimer's disease.
  • Targeting U1 snRNA function presents a novel therapeutic strategy for AD.