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

Bone marrow B lymphocyte development in c-abl-deficient mice

J D Hardin1, S Boast, P L Schwartzberg

  • 1Department of Biochemistry and Molecular Biophysics, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA.

Cellular Immunology
|October 1, 1995
PubMed
Summary

The c-abl tyrosine kinase gene mutation causes varied defects in B cell development in mice. These findings suggest c-Abl signaling is crucial for early B cell stages.

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

SIRT6 in DNA repair, metabolism and ageing.

Journal of internal medicine·2008
Same author

Integrative analysis reveals 53BP1 copy loss and decreased expression in a subset of human diffuse large B-cell lymphomas.

Oncogene·2007
Same author

The interplay between nonhomologous end-joining and cell cycle checkpoint factors in development, genomic stability, and tumorigenesis.

Cold Spring Harbor symposia on quantitative biology·2003
Same author

Impaired nonhomologous end-joining provokes soft tissue sarcomas harboring chromosomal translocations, amplifications, and deletions.

Molecular cell·2002
Same author

Increased accumulation of hybrid V(D)J joins in cells expressing truncated versus full-length RAGs.

Molecular cell·2002
Same author

TRAF1 is a negative regulator of TNF signaling. enhanced TNF signaling in TRAF1-deficient mice.

Immunity·2001

Area of Science:

  • Hematology
  • Immunology
  • Molecular Biology

Background:

  • The c-abl tyrosine kinase gene plays a role in cellular signaling pathways.
  • Mutations in c-abl can lead to various developmental abnormalities.

Purpose of the Study:

  • To investigate the role of c-Abl signaling in B cell development.
  • To characterize the hematopoietic defects in c-abl mutant mice.

Main Methods:

  • Flow cytometry (FACS) analysis of bone marrow from c-abl mutant mice.
  • Assessment of B cell precursor responses to various cytokines.
  • Bone marrow and fetal liver cell transfer experiments.

Main Results:

  • C-abl mutant mice exhibit variable reductions in pro-B and pre-B cells, impacting B cell development stages.

Related Experiment Videos

  • B cell precursor response to interleukin-7 is variably affected, while responses to other cytokines remain normal.
  • Hematopoietic defects are transferable via adult bone marrow but not fetal liver.

    • Conclusions:

    • C-Abl signaling pathways are critical for early B cell development in a stage-specific manner.
    • Despite variable defects, the overall hematopoietic system in c-abl mutant mice remains largely intact.