rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
10
|
pubmed:dateCreated |
2001-5-22
|
pubmed:abstractText |
Bruton's tyrosine kinase (Btk) is a nonreceptor tyrosine kinase involved in precursor B (pre-B) cell receptor signaling. Here we demonstrate that Btk-deficient mice have an approximately 50% reduction in the frequency of immunoglobulin (Ig) lambda light chain expression, already at the immature B cell stage in the bone marrow. Conversely, transgenic mice expressing the activated mutant Btk(E41K) showed increased lambda usage. As the kappa/lambda ratio is dependent on (a) the level and kinetics of kappa and lambda locus activation, (b) the life span of pre-B cells, and (c) the extent of receptor editing, we analyzed the role of Btk in these processes. Enforced expression of the Bcl-2 apoptosis inhibitor did not alter the Btk dependence of lambda usage. Crossing 3-83mudelta autoantibody transgenic mice into Btk-deficient mice showed that Btk is not essential for receptor editing. Also, Btk-deficient surface Ig(+) B cells that were generated in vitro in interleukin 7-driven bone marrow cultures manifested reduced lambda usage. An intrinsic defect in lambda locus recombination was further supported by the finding in Btk-deficient mice of reduced lambda usage in the fraction of pre-B cells that express light chains in their cytoplasm. These results implicate Btk in the regulation of the activation of the lambda locus for V(D)J recombination in pre-B cells.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/11369788-10196179,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11369788-10220140,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/11369788-9858590
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
May
|
pubmed:issn |
0022-1007
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pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
21
|
pubmed:volume |
193
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1169-78
|
pubmed:dateRevised |
2011-11-2
|
pubmed:meshHeading |
pubmed-meshheading:11369788-Animals,
pubmed-meshheading:11369788-Antigens, CD19,
pubmed-meshheading:11369788-B-Lymphocytes,
pubmed-meshheading:11369788-Bone Marrow Cells,
pubmed-meshheading:11369788-Enzyme Activation,
pubmed-meshheading:11369788-Female,
pubmed-meshheading:11369788-Gene Rearrangement, B-Lymphocyte, Light Chain,
pubmed-meshheading:11369788-Genes, bcl-2,
pubmed-meshheading:11369788-Hematopoietic Stem Cells,
pubmed-meshheading:11369788-Mice,
pubmed-meshheading:11369788-Protein-Tyrosine Kinases,
pubmed-meshheading:11369788-RNA Editing,
pubmed-meshheading:11369788-Receptors, Antigen, B-Cell
|
pubmed:year |
2001
|
pubmed:articleTitle |
Bruton's tyrosine kinase regulates the activation of gene rearrangements at the lambda light chain locus in precursor B cells in the mouse.
|
pubmed:affiliation |
Department of Immunology, Faculty of Medicine, Erasmus University Rotterdam, 3000 DR Rotterdam, The Netherlands.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|