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

Gradient of E2A activity in B-cell development.

Sabine Herblot1, Peter D Aplan, Trang Hoang

  • 1The Clinical Research Institute of Montréal, Montréal, Québec, Canada.

Molecular and Cellular Biology
|January 11, 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

Bridging the Funding Gap in Drug Development for Amyotrophic Lateral Sclerosis.

Neurology. Clinical practice·2026
Same author

A Chemical-Genetic Interaction Matrix Reveals Drug Mechanism and Genetic Architecture.

bioRxiv : the preprint server for biology·2026
Same author

Inhibition of PAK2 in endothelial cells suppresses tumor angiogenesis and promotes immune sensitization through CXCL10.

Cell reports·2025
Same author

Azanucleoside treatment leads to B-cell precursor acute lymphoblastic leukemia.

Blood neoplasia·2025
Same author

5-Azacytidine and decitabine induce C > G transversions in both murine and human cells.

Leukemia·2025
Same author

Disruption of normal stem cell function and transmission of myelodysplastic syndrome by self-renewal of committed myeloid lineage cells.

Stem cell reports·2025
Same journal

Aberrant Expression of miR-25-3p/EZH2 Is Involved in T Cell Activation in Aplastic Anemia.

Molecular and cellular biology·2026
Same journal

Characterization of the m<sup>6</sup>A Epitranscriptome in Fibroblast Senescence.

Molecular and cellular biology·2026
Same journal

Insights into FACT in Cancers with Targeted Therapeutic Implications.

Molecular and cellular biology·2026
Same journal

Human lncRNA, hLinfRNA7 (IDO1-AS) Regulates Cytokine Expression, Tryptophan Catabolism, and Inflammatory Response in Macrophage.

Molecular and cellular biology·2026
Same journal

mTORC1-Dependent Regulation of the CCL24-CCR3 Axis Controls Granuloma Formation and Maintenance in Sarcoidosis.

Molecular and cellular biology·2026
Same journal

The Novel Compound SIC-19 Triggers CUL4B-Mediated Ubiquitination and Degradation of SIK2.

Molecular and cellular biology·2026
See all related articles

The E2A gene is crucial for B-cell development and has an antiproliferative role in early B-cell progenitors. Its reduced function contributes to B-cell acute lymphoblastic leukemia (B-ALL) by affecting cell growth and differentiation.

Area of Science:

  • Hematology
  • Molecular Biology
  • Genetics

Background:

  • The E2A gene encodes transcription factors E12 and E47, vital for B-cell differentiation.
  • E2A haplo-insufficiency disrupts B-cell development checkpoints, including lineage commitment and immunoglobulin M expression.
  • Chromosomal translocations targeting E2A are common in B-cell acute lymphoblastic leukemia (B-ALL).

Purpose of the Study:

  • To investigate the role of E2A gene dosage in B-cell progenitor proliferation and differentiation.
  • To explore the functional relationship between E2A and SCL/Tal1 in B-cell development.
  • To elucidate E2A's contribution to leukemogenesis in B-ALL.

Main Methods:

  • Analysis of B-cell populations in E2A(+/-) and wild-type mice.
  • Assessment of cell cycle status and p21(waf/cip1) levels in B-cell progenitors.

Related Experiment Videos

  • Ectopic expression studies of SCL/Tal1 in the B-cell lineage.

    • Main Results:

    • E2A haplo-insufficient pro-B cells exhibit increased cell cycle progression, correlated with lower p21(waf/cip1) levels, indicating an antiproliferative function.
    • Ectopic SCL/Tal1 expression blocks B-cell lineage commitment and exacerbates E2A haplo-insufficiency, suggesting genetic interaction.
    • Evidence supports a model of increasing E2A activity from pre-pro-B to pre-B stages, regulating both cell growth and differentiation.

    Conclusions:

    • E2A plays a dual role: controlling cell proliferation at low levels and promoting differentiation at high levels.
    • Disruption of E2A alleles contributes to B-ALL pathogenesis, alongside oncogenic fusion proteins.
    • Understanding E2A dosage effects is critical for B-cell development and leukemia research.