Publication Date:
1999-01-15
Description:
Mice with a targeted gene disruption of p85alpha, a regulatory subunit of phosphoinositide 3-kinase, had impaired B cell development at the pro-B cell stage, reduced numbers of mature B cells and peritoneal CD5+ Ly-1 B cells, reduced B cell proliferative responses, and no T cell-independent antibody production. These phenotypes are nearly identical to those of Btk-/- or xid (X-linked immunodeficiency) mice. These results provide evidence that p85alpha is functionally linked to the Btk pathway in antigen receptor-mediated signal transduction and is pivotal in B cell development and functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suzuki, H -- Terauchi, Y -- Fujiwara, M -- Aizawa, S -- Yazaki, Y -- Kadowaki, T -- Koyasu, S -- New York, N.Y. -- Science. 1999 Jan 15;283(5400):390-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9888854" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
Antibody Formation
;
Antigens, CD5/analysis
;
Antigens, Ly/analysis
;
Antigens, T-Independent/immunology
;
B-Lymphocyte Subsets/cytology/immunology
;
B-Lymphocytes/cytology/*immunology
;
Bone Marrow/immunology
;
Cell Survival
;
Gene Targeting
;
Genetic Linkage
;
Immunologic Deficiency Syndromes/*enzymology/genetics/immunology
;
Lymphocyte Count
;
Lymphoid Tissue/immunology
;
Mice
;
Mutation
;
Phenotype
;
Phosphatidylinositol 3-Kinases/genetics/*metabolism
;
Protein-Tyrosine Kinases/genetics/metabolism
;
Signal Transduction
;
T-Lymphocytes/immunology
;
X Chromosome
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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