Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6554
pubmed:dateCreated
1995-12-15
pubmed:databankReference
pubmed:abstractText
The tyrosine kinase Syk (relative molecular mass 72,000), which is widely expressed in haematopoietic cells, becomes associated with and activated by engagement of the B-cell antigen receptor. Furthermore, it has been implicated in signalling through the receptors for interleukin-2 (IL-2), granulocyte colony-stimulating factor (G-CSF) and Fc, the T cell receptor, as well as through receptors for several platelet agonists. A homologous kinase, ZAP-70, is crucial in signalling through the T-cell receptor and in T-cell development. Using homologous recombination in embryonic stem cells, we created mice null for the syk gene which showed petechiae in utero and died shortly after birth. Irradiated mice reconstituted with Syk-deficient fetal liver showed a block in B-cell development at the pro-B to pre-B cell transition, consistent with a key role for Syk in pre-B-cell receptor signalling. Despite the production of small numbers of immature B cells, Syk-deficient radiation chimaeras failed to accumulate mature B cells, indicating a possible role for this protein in the production or maintenance of mature B cells. In addition, whereas the development of alpha beta T cells proceeded normally, Syk-deficient mice showed impaired development of thymocytes using the V gamma 3 variable region gene (V gamma 3+ thymocytes). Finally, we show that Syk is not required for signalling through the IL-2 and G-CSF receptors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0028-0836
pubmed:author
pubmed:issnType
Print
pubmed:day
16
pubmed:volume
378
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
298-302
pubmed:dateRevised
2011-11-2
pubmed:meshHeading
pubmed-meshheading:7477352-Amino Acid Sequence, pubmed-meshheading:7477352-Animals, pubmed-meshheading:7477352-Animals, Newborn, pubmed-meshheading:7477352-B-Lymphocytes, pubmed-meshheading:7477352-Cell Differentiation, pubmed-meshheading:7477352-Cell Line, pubmed-meshheading:7477352-Cells, Cultured, pubmed-meshheading:7477352-Chimera, pubmed-meshheading:7477352-Crosses, Genetic, pubmed-meshheading:7477352-Enzyme Precursors, pubmed-meshheading:7477352-Female, pubmed-meshheading:7477352-Intracellular Signaling Peptides and Proteins, pubmed-meshheading:7477352-Liver, pubmed-meshheading:7477352-Mice, pubmed-meshheading:7477352-Mice, Inbred C57BL, pubmed-meshheading:7477352-Molecular Sequence Data, pubmed-meshheading:7477352-Mutagenesis, pubmed-meshheading:7477352-Protein-Tyrosine Kinases, pubmed-meshheading:7477352-Purpura, pubmed-meshheading:7477352-T-Lymphocytes, pubmed-meshheading:7477352-ZAP-70 Protein-Tyrosine Kinase
pubmed:year
1995
pubmed:articleTitle
Perinatal lethality and blocked B-cell development in mice lacking the tyrosine kinase Syk.
pubmed:affiliation
National Institute for Medical Research, Mill Hill, London, UK.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't