Deutsch
 
Benutzerhandbuch Datenschutzhinweis Impressum Kontakt
  DetailsucheBrowse

Datensatz

DATENSATZ AKTIONENEXPORT

Freigegeben

Zeitschriftenartikel

Functional analysis of Ig-α signaling in the context of B cell development and response

MPG-Autoren
/persons/resource/persons191156

Klingmueller,  Ursula
Spemann Laboratory, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

/persons/resource/persons191285

Reth,  Michael
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

/persons/resource/persons191264

Pelanda,  Roberta
Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Externe Ressourcen
Es sind keine Externen Ressourcen verfügbar
Volltexte (frei zugänglich)
Es sind keine frei zugänglichen Volltexte verfügbar
Ergänzendes Material (frei zugänglich)
Es sind keine frei zugänglichen Ergänzenden Materialien verfügbar
Zitation

Thiemann, S., Klingmueller, U., Reth, M., & Pelanda, R. (2003). Functional analysis of Ig-α signaling in the context of B cell development and response. FASEB Journal, 17(7 Suppl. Suppl. S), C97-C97.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-002B-9549-A
Zusammenfassung
The B cell antigen receptor (BCR) signaling cascade is initiated by phosphorylation of tyrosine residues in the Immunoreceptor Tyrosine based Activation Motif (ITAM) of Ig-α and Ig-β. Signals initiated by the pre-BCR in pre-B cells and the BCR in immature and mature cells can lead to cell maturation, selection, terminal differentiation or cell death. It is still unclear how a single receptor can mediate such a variety of cellular responses. Our aim is to develop a system for the structural and functional analysis of Ig-α in vivo and to understand its role in B cell development, selection and response. We use retroviral gene transfer to introduce different mb-1 (Ig-α encoding gene) mutants into hematopoietic stem cells of Ig-α-deficient mice. Transduced cells are reinjected into irradiated recipient mice where they can differentiate into B cells. Here we have focused on the serine and threonine residues of the cytoplasmic region of Ig-α. These residues are phosphorylated upon BCR engagement and studies in cell lines indicated their potential negative regulatory role in BCR signaling. We found that Ig-α deficient hematopoietic stem cells transduced with retroviral vectors containing either the wild-type or a serine/threonine mutated mb-1 sequence were able to differentiate into IgM expressing cells in vivo. Thus, our data indicate that the serine and threonine residues do not play a dominant role in pre-BCR signaling as pre-B cells and immature B cells expressing serine and treonine mutant Ig-α develop. We are in the process of testing the effect of these mutations in B cell negative selection and B cell response.