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           Search results for: Anti BLK( B lymphoid tyrosine kinase)   

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#25972485   2015/06/06 Save this To Up

Concordance of increased B1 cell subset and lupus phenotypes in mice and humans is dependent on BLK expression levels.

Polymorphisms in the B lymphoid tyrosine kinase (BLK) gene have been associated with autoimmune diseases, including systemic lupus erythematosus, with risk correlating with reduced expression of BLK. How reduced expression of BLK causes autoimmunity is unknown. Using Blk(+/+) , Blk(+/-) , and Blk(-/-) mice, we show that aged female Blk(+/-) and Blk(-/-) mice produced higher anti-dsDNA IgG Abs and developed immune complex-mediated glomerulonephritis, compared with Blk(+/+) mice. Starting at young age, Blk(+/-) and Blk(-/-) mice accumulated increased numbers of splenic B1a cells, which differentiated into class-switched CD138(+) IgG-secreting B1a cells. Increased infiltration of B1a-like cells into the kidneys was also observed in aged Blk(+/-) and Blk(-/-) mice. In humans, we found that healthy individuals had BLK genotype-dependent levels of anti-dsDNA IgG Abs as well as increased numbers of a B1-like cell population, CD19(+)CD3(-)CD20(+)CD43(+)CD27(+), in peripheral blood. Furthermore, we describe the presence of B1-like cells in the tubulointerstitial space of human lupus kidney biopsies. Taken together, our study reveals a previously unappreciated role of reduced BLK expression on extraperitoneal accumulation of B1a cells in mice, as well as the presence of IgG autoantibodies and B1-like cells in humans.

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#20861858   2011/03/03 Save this To Up

Association of EBF1, FAM167A(C8orf13)-BLK and TNFSF4 gene variants with primary Sjögren's syndrome.

We performed a candidate gene association study in 540 patients with primary Sjögren's Syndrome (SS) from Sweden (n=344) and Norway (n=196) and 532 controls (n=319 Swedish, n=213 Norwegian). A total of 1139 single-nucleotide polymorphisms (SNPs) in 84 genes were analyzed. In the meta-analysis of the Swedish and Norwegian cohorts, we found high signals for association between primary SS and SNPs in three gene loci, not previously associated with primary SS. These are the early B-cell factor 1 (EBF1) gene, P=9.9 × 10(-5), OR 1.68, the family with sequence similarity 167 member A-B-lymphoid tyrosine kinase (FAM167A-BLK) locus, P=4.7 × 10(-4), OR 1.37 and the tumor necrosis factor superfamily (TNFSF4=Ox40L) gene, P=7.4 × 10(-4), OR 1.34. We also confirmed the association between primary SS and the IRF5/TNPO3 locus and the STAT4 gene. We found no association between the SNPs in these five genes and the presence of anti-SSA/anti-SSB antibodies. EBF1, BLK and TNFSF4 are all involved in B-cell differentiation and activation, and we conclude that polymorphisms in several susceptibility genes in the immune system contribute to the pathogenesis of primary SS.

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#19796918   2010/02/15 Save this To Up

Association of the C8orf13-BLK region with systemic sclerosis in North-American and European populations.

Genetic studies in the systemic sclerosis (SSc), an autoimmune disease that clinically manifests with dermal and internal organ fibrosis and small vessel vasculopathy, have identified multiple susceptibility genes including HLA-class II, PTPN22, IRF5, and STAT4 which have also been associated with other autoimmune diseases, such as systemic lupus erythematosus (SLE). These data suggest that there are common autoimmune disease susceptibility genes. The current report sought to determine if polymorphisms in the C8orf13-BLK region (chromosome 8p23.1-B lymphoid tyrosine kinase), which is associated with SLE, are associated also with SSc.

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#8195169   1994/06/29 Save this To Up

Specific recognition of the blk promoter by the B-lymphoid transcription factor B-cell-specific activator protein.

Several genes of the src family encode protein-tyrosine kinases that associate with the B-cell antigen receptor complex and are activated upon receptor cross-linking, including blk, lyn, and fyn. The blk gene is the only member of this family whose expression is restricted to B-lymphoid cells. In the B lineage, blk is developmentally regulated: blk transcripts are first detected in pro-B-cells and persist until the differentiation of mature B-cells to plasma cells. We have found that the blk promoter is a target for a specific DNA-binding protein whose activity in B-lymphoid cell lines is positively correlated with blk expression. By three criteria, we have identified this DNA-binding protein as the transcription factor B-cell-specific activator protein (BSAP): 1) oligonucleotides containing known BSAP recognition sites were found to compete specifically with blk for binding to the protein detected in B-lymphoid extracts; 2) authentic BSAP was shown to bind the same site within the blk promoter as the protein identified in B-lymphoid extracts; and 3) the specific DNA-protein complex formed in B-lymphoid extracts was shown to react with an anti-BSAP antiserum. BSAP has been implicated previously in the transcriptional regulation of CD19, whose pattern of expression in B-cell development coincides with that of blk. These observations, and the correlation between expression of BSAP and expression of blk, suggest that BSAP is a positive regulator of blk transcription.

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#7514299   1994/06/16 Save this To Up

Tyrosine phosphorylation of Blk and Fyn Src homology 2 domain-binding proteins occurs in response to antigen-receptor ligation in B cells and constitutively in pre-B cells.

Proteins that bind to discrete domains of the Blk, Fyn, Lyn, and Btk protein tyrosine kinases were examined in pre-B cells that had not been subjected to any external stimulation, as well as in nonstimulated and antigen-receptor-ligated B cells. Proteins that bind to the Src homology 2 domains of Blk and Fyn were identified in B cells that had been activated with anti-IgM but were not identified in unstimulated B cells. A number of Blk and Fyn Src homology 2 domain-binding phosphoproteins were also observed in pre-B cells that had not been stimulated in vitro. The phosphoproteins seen in activated B cells potentially represent substrates that play a role in the pathway of antigen-receptor-mediated signaling. Distinct signaling pathways involving distinguishable kinase substrates may be relevant in pre-B-cell-receptor-mediated cell survival during ontogeny. These results indirectly support models that predict constitutive ligand-independent signaling by the pre-antigen receptor during lymphoid ontogeny.

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#1378935   1992/08/26 Save this To Up

Examination of B lymphoid cell lines for membrane immunoglobulin-stimulated tyrosine phosphorylation and src-family tyrosine kinase mRNA expression.

Crosslinking of membrane immunoglobulin (mIg) on B cells induces two signal transduction pathways: protein tyrosine phosphorylation and phosphoinositide turnover. A panel of murine and human B cell-lines, representing different stages of B cell development, was examined for the presence of anti-immunoglobulin-induced protein tyrosine phosphorylation. Of 10 B cell lines examined, only one, the human Raji cell line, had no detectably induced protein tyrosine phosphorylation. The pattern of proteins that were phosphorylated on tyrosine in response to mIg crosslinking differed somewhat in cell lines representing different stages of B cell development. Differences in the levels of constitutive phosphorylation of proteins were also observed between the cell lines. The identity of the tyrosine kinase(s) activated by membrane immunoglobulin ligation is not known. However, members of the src family of intracellular tyrosine kinases have been implicated as signal transduction molecules. As the tyrosine phosphorylation of proteins is a general phenomenon of signal transduction by membrane immunoglobulin, the tyrosine kinase(s) activated by it might be expected to be present in all cell lines in which the tyrosine phosphorylation signalling occurs. Therefore we examined these B cells for expression of mRNAs encoding the eight known src-like tyrosine kinases. Surprisingly, all eight kinase mRNAs were expressed in at least some of the B cell lines examined. The expression pattern of the fyn, hck, and lck genes suggests that expression of these kinases may be developmentally regulated in the B cell lineage. Three of the kinases, p55blk, p53/p56lyn and p60src, were detected in all 10 B cell lines. Whereas the src gene shows a ubiquitous pattern of expression, the expression of the blk and lyn genes is mostly restricted to cells of hematopoietic origin, and more especially B lymphoid cells. Thus, p55blk and p53/p56lyn may be particularly good candidates for the membrane immunoglobulin-activated tyrosine kinase.

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#1537861   1992/04/02 Save this To Up

Structure and developmental regulation of the B-lymphoid tyrosine kinase gene blk.

The murine blk gene, which encodes a B-lymphoid-specific tyrosine kinase of the Src family (p55blk), contains 13 exons that span more than 30 kilobases of DNA on chromosome 14. In the first three exons, which encode the 5'-untranslated region and N-terminal amino acid sequence unique to p55blk, the blk gene differs from other members of the src family; in the last 10 exons, the organization of the blk gene is similar to that of other src genes. By primer extension and S1 nuclease protection analyses, we show that blk transcripts initiate from four major sites at the 5'-flank of blk; two sites predominate. The resulting transcripts differ only in the lengths of their 5'-untranslated sequences and encode identical proteins. None of the transcriptional start sites are preceded by consensus TATA elements, AT-rich elements, or extensive GC-rich regions. Expression of blk is regulated during B-cell development: blk RNA is expressed in all pro-B-, pre-B-, and mature B-cell lines examined, but is absent from plasma cell lines. Immunolocalization of p55blk in normal mouse spleen supports these observations: staining is restricted to lymphocytes and is concentrated in regions rich in B-cells; plasma cells and stromal cells are not stained with anti-Blk antibodies. Assays for RNA synthesis in isolated nuclei indicate that the lineage and developmental stage specificities of blk expression are regulated at least in part by changes in its rate of transcription.

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