Return to search

Biochemical basis of B cell dysfunction in Lyn kinase deficient mice

B lymphocytes constitutes an important arm of the immune system, and their response to antigen is largely dependent upon signal transduction through the B cell receptor (BCR). Such a potent receptor, however, needs to be further balanced by positive and negative regulators to prevent harmful effects that may arise from inappropriate stimulation. Src family protein tyrosine kinase Lyn is involved in both positive and negative regulation, since the both gain-of-function Lyn and loss-of-function Lyn mutations caused autoimmunity in mice. The exact signalling pathway(s) regulated by Lyn in B cells, however, are still not clear. Work presented in this thesis attempts to elucidate the biochemical mechanisms that underline the double-edged nature of Lyn in BCR signalling. (For complete abstract open document)

Identiferoai:union.ndltd.org:ADTP/245596
CreatorsXu, Yuekang
Source SetsAustraliasian Digital Theses Program
LanguageEnglish
Detected LanguageEnglish
RightsTerms and Conditions: Copyright in works deposited in the University of Melbourne Eprints Repository (UMER) is retained by the copyright owner. The work may not be altered without permission from the copyright owner. Readers may only, download, print, and save electronic copies of whole works for their own personal non-commercial use. Any use that exceeds these limits requires permission from the copyright owner. Attribution is essential when quoting or paraphrasing from these works., Open Access

Page generated in 0.0021 seconds