Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Search research articles

Related Experiment Videos

Multiple cis elements regulate an alternative splicing event at 4.1R pre-mRNA during erythroid differentiation.

M Deguillien¹, S C Huang, M Morinière

¹Centre de Génétique Moléculaire et Cellulaire, CNRS UMR 5534, Université Lyon 1, Villeurbanne, France.

|December 12, 2001

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

JAK2V617F mRNA metabolism in myeloproliferative neoplasm cell lines.

Blood cancer journal·2014

Same author

Pulmonary embolism by amniotic fluid; report of three cases with a new diagnostic procedure.

Surgery, gynecology & obstetrics·2010

Same author

Subtle distinct regulations of late erythroid molecular events by PI3K/AKT-mediated activation of Spi-1/PU.1 oncogene autoregulation loop.

Oncogene·2010

Same author

Comprehensive cancer centres and the war on cancer.

Nature reviews. Cancer·2002

Same author

Reassignment of the EPB4.1 gene to 1p36 and assessment of its involvement in neuroblastomas.

European journal of clinical investigation·2001

Same author

A missense mutation (Q279R) in the fumarylacetoacetate hydrolase gene, responsible for hereditary tyrosinemia, acts as a splicing mutation.

BMC genetics·2001

Same journal

Fibrocytes drive JAK2V617F-mutated myelofibrosis: pitavastatin reverses marrow fibrosis and anemia.

Blood·2026

Same journal

Identifying steroid-refractory aGVHD before it happens.

Blood·2026

Same journal

ELISA-negative HIT: antibody recognition and relevance.

Blood·2026

Same journal

EBV and immunodeficiency: the odd couple drawn to the brain.

Blood·2026

Same journal

A bone to pick with ferric carboxymaltose.

Blood·2026

Same journal

A step toward streamlining HIT diagnosis.

Blood·2026

See all related articles

Exon 16 inclusion in protein 4.1R messenger RNA (mRNA) is vital for red blood cell membrane formation. Regulatory elements within the gene control this splicing event during erythroid development.

Area of Science:

Molecular Biology
Cell Biology
Genetics

Background:

Protein 4.1R is crucial for red blood cell membrane stability.
Exon 16 inclusion in protein 4.1R mRNA is essential for erythroid development.
Splicing regulation of exon 16 is key to proper protein 4.1R function.

Purpose of the Study:

To investigate the cis-acting regulatory sequences controlling exon 16 splicing in protein 4.1R.
To establish a model system for studying erythroid-specific splicing.
To understand the molecular mechanisms behind exon 16 inclusion during erythroid differentiation.

Main Methods:

Transfection of a minigene into murine erythroleukemia cells.
Analysis of splicing patterns before and after induction of differentiation.

Related Experiment Videos

Systematic deletion and mutation analysis of cis-acting elements in introns and exon.

Main Results:

The upstream intron contains distal and proximal enhancer elements for exon recognition.
The exon itself harbors a constitutive splicing silencer and a weak 5' splice site.
The downstream intron possesses enhancer elements, including UGCAUG motifs, active during differentiation.

Conclusions:

A balance of positive and negative regulatory elements governs exon 16 splicing.
Activation of enhancer elements during late erythroid differentiation promotes exon 16 inclusion.
These findings elucidate the regulatory network controlling protein 4.1R mRNA processing in red blood cells.