ArticleProceedings of the National Academy of Sciences of the United States of America1993
Antisense oligodeoxynucleotides to the blk tyrosine kinase prevent anti-mu-chain-mediated growth inhibition and apoptosis in a B-cell lymphoma.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 48 citations in OpenAlex.
- Hygiene Hypothesis as the Etiology of Kawasaki Disease: Dysregulation of Early B Cell Development.International journal of molecular sciences · 2021Review
- The autoimmunity-associated BLK haplotype exhibits cis-regulatory effects on mRNA and protein expression that are prominently observed in B cells early in development.Human molecular genetics · 2012Article
- Association of the C8orf13-BLK region with systemic sclerosis in North-American and European populations.Journal of autoimmunity · 2010Article
- Clinical stage EGFR inhibitors irreversibly alkylate Bmx kinase.Bioorganic & medicinal chemistry letters · 2008Article
- Review
- The B-cell-specific Src-family kinase Blk is dispensable for B-cell development and activation.Molecular and cellular biology · 2000Article
- Role of protein kinase activity in apoptosis.Experientia · 1996Review
- Connections between signal transduction components and cellular responses initiated by antigen receptor on B lymphocytes.The Journal of experimental medicine · 1995Article
- Antigen-receptor induced clonal expansion and deletion of lymphocytes are impaired in mice lacking HS1 protein, a substrate of the antigen-receptor-coupled tyrosine kinases.The EMBO journal · 1995Article
- Restoration of surface IgM-mediated apoptosis in an anti-IgM-resistant variant of WEHI-231 lymphoma cells by HS1, a protein-tyrosine kinase substrate.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
- Protein-tyrosine phosphorylation regulates apoptosis in human eosinophils and neutrophils.Proceedings of the National Academy of Sciences of the United States of America · 1994Article
- Temporal differences in the activation of three classes of non-transmembrane protein tyrosine kinases following B-cell antigen receptor surface engagement.Proceedings of the National Academy of Sciences of the United States of America · 1994Article
- 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.Proceedings of the National Academy of Sciences of the United States of America · 1994Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Crosslinking of membrane immunoglobulin (mIg) receptors by anti-Ig causes growth inhibition and subsequent cell death due to apoptosis in a murine B-cell lymphoma model. The earliest signal transduction via mIg has recently been shown to be dependent on the activation of one or more protein tyrosine kinases (PTKs). In this study, we utilized the CH31 lymphoma, which is extremely sensitive to growth inhibition by anti-Ig, to examine the role of PTKs in cell cycle arrest. This cell line expresses multiple PTKs, whose activities are stimulated by crosslinking mIg. To determine whether PTK activity is essential for the inhibition of cell growth, we exposed CH31 cells to antisense oligodeoxynucleotides for the blk PTK prior to the growth inhibition assay. We found that exposure of CH31 cells to blk antisense effectively prevented anti-mu-chain-mediated growth inhibition and subsequent apoptosis. Corresponding blk sense or antisense oligonucleotides for other PTKs had no protective effect against anti-mu. Moreover, antisense blk oligonucleotides had no effect on transforming growth factor beta-mediated growth arrest and apoptosis. Further experiments showed significantly reduced endogenous p55blk in blk antisense-treated cells. In addition, anti-mu stimulation of antisense-treated cells failed to induce any detectable increase in kinase activity of p55blk, a result suggesting the uncoupling of blk proteins from normal signal pathways that are essential for growth inhibition. These results implicate a role of blk kinase in anti-mu-mediated pathway to cell cycle arrest.
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