scholarly journals B Cell Receptor (BCR) Cross-Talk: IL-4 Creates an Alternate Pathway for BCR-Induced ERK Activation That Is Phosphatidylinositol 3-Kinase Independent

2005 ◽  
Vol 174 (9) ◽  
pp. 5375-5381 ◽  
Author(s):  
Benchang Guo ◽  
Thomas L. Rothstein
2007 ◽  
Vol 178 (10) ◽  
pp. 6332-6341 ◽  
Author(s):  
Laurent Verkoczy ◽  
Bao Duong ◽  
Patrick Skog ◽  
Djemel Aït-Azzouzene ◽  
Kamal Puri ◽  
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2009 ◽  
Vol 284 (15) ◽  
pp. 9804-9813 ◽  
Author(s):  
Yasuhiro Imamura ◽  
Akihisa Oda ◽  
Takashi Katahira ◽  
Kenji Bundo ◽  
Kelly A. Pike ◽  
...  

2002 ◽  
Vol 196 (6) ◽  
pp. 753-763 ◽  
Author(s):  
Elizabeth Clayton ◽  
Giuseppe Bardi ◽  
Sarah E. Bell ◽  
David Chantry ◽  
C. Peter Downes ◽  
...  

Mice lacking the p110δ catalytic subunit of phosphatidylinositol 3-kinase have reduced numbers of B1 and marginal zone B cells, reduced levels of serum immunoglobulins, respond poorly to immunization with type II thymus-independent antigen, and are defective in their primary and secondary responses to thymus-dependent antigen. p110δ−/− B cells proliferate poorly in response to B cell receptor (BCR) or CD40 signals in vitro, fail to activate protein kinase B, and are prone to apoptosis. p110δ function is required for BCR-mediated calcium flux, activation of phosphlipaseCγ2, and Bruton's tyrosine kinase. Thus, p110δ plays a critical role in B cell homeostasis and function.


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