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

Decrease in hnRNP A/B expression during erythropoiesis mediates a pre-mRNA splicing switch.

Victor C Hou1, Robert Lersch, Sherry L Gee

  • 1Life Sciences Division, Lawrence Berkeley National Laboratory, University of California at Berkeley, Berkeley, CA 94720, USA.

The EMBO Journal
|November 12, 2002
PubMed
Summary
This summary is machine-generated.

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

Punctate Intramural Gastric Calcifications Reveal Diffuse-Type Adenocarcinoma in Asymptomatic Iron Deficiency Anemia.

Gastro hep advances·2026
Same author

MYC-Mediated USP39 Upregulation Stabilizes SRSF1 in Pancreatic Cancer.

Molecular cancer research : MCR·2026
Same author

AAAAI physician survey: Current antihistamine use in the clinical setting.

The journal of allergy and clinical immunology. Global·2026
Same author

Heat Vulnerability and Community Resilience: A Survey Analysis in Dallas, Texas.

Journal of primary care & community health·2026
Same author

ASO-based PKM splice-switching therapy increases anti-CTLA-4 antibody efficacy in pancreatic ductal adenocarcinoma.

Cell discovery·2026
Same author

Exon-Skipping Antisense Oligonucleotides for H3.3K27M-Altered Diffuse Midline Glioma Therapy.

bioRxiv : the preprint server for biology·2026
Same journal

Scalable phosphotyrosine enrichment with SH2 superbinder enables deep profiling of EGF responses.

The EMBO journal·2026
Same journal

Essential nucleus-apical pole linkage maintains division fidelity during Plasmodium progeny formation.

The EMBO journal·2026
Same journal

From cell atlases to mechanisms: bridging scRNA-seq discovery with in vivo genetics.

The EMBO journal·2026
Same journal

Mitochondrial calcium regulates lipid metabolism by modulating tethering of mitochondria to lipid droplets.

The EMBO journal·2026
Same journal

Chromosome condensation mechanically primes the nucleus for mitosis.

The EMBO journal·2026
Same journal

NDR kinase SAX-1 controls dendrite branch-specific elimination during neuronal remodeling in C. elegans.

The EMBO journal·2026
See all related articles

Protein 4.1R exon 16 (E16) splicing is crucial for red blood cell membrane integrity. hnRNP A/B proteins bind to a silencer element (CE16) to repress E16 splicing during early erythropoiesis.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Alternative pre-mRNA splicing is a key regulatory mechanism in gene expression.
  • Proper erythrocyte membrane integrity is essential for red blood cell function and survival.
  • Protein 4.1R plays a critical role in red blood cell structure and stability.

Purpose of the Study:

  • To investigate the molecular mechanisms regulating protein 4.1R exon 16 (E16) splicing during erythropoiesis.
  • To identify regulatory elements and protein factors involved in E16 splicing control.
  • To understand the physiological significance of E16 splicing in red blood cell development.

Main Methods:

  • Identification and characterization of exonic splicing silencer elements (CE16) in protein 4.1R E16.

Related Experiment Videos

  • RNA-protein interaction studies using affinity selection assays to identify hnRNP A/B binding.
  • Pre-mRNA splicing assays with model substrates to assess the function of CE16.
  • Protein depletion and repletion experiments using nuclear extracts and recombinant proteins.
  • Analysis of hnRNP A/B protein expression during mouse erythroblast differentiation.

    • Main Results:

    • A conserved exonic splicing silencer (CE16) in protein 4.1R E16 was identified.
    • hnRNP A/B proteins were found to bind specifically to CE16 and repress E16 splicing.
    • Mutagenesis or replacement of CE16 relieved splicing repression.
    • Depletion of hnRNP A/B increased E16 inclusion, while repletion restored silencing.
    • hnRNP A/B protein expression decreased during mouse erythroblast differentiation, coinciding with E16 splicing activation.

    Conclusions:

    • hnRNP A/B proteins, through interaction with CE16, act as repressors of protein 4.1R E16 splicing during early erythropoiesis.
    • Developmental down-regulation of hnRNP A/B proteins facilitates the activation of the E16 splicing switch.
    • This regulated splicing event is critical for establishing the mechanical integrity of the erythrocyte membrane.