دورية أكاديمية
Transgene expression of bcl-xL permits anti-immunoglobulin (Ig)-induced proliferation in xid B cells.
| العنوان: | Transgene expression of bcl-xL permits anti-immunoglobulin (Ig)-induced proliferation in xid B cells. |
|---|---|
| المؤلفون: | Solvason N; Department of Immunology, DNAX Research Institute, Palo Alto, California 94304, USA. nsolvason@anergen.com, Wu WW, Kabra N, Lund-Johansen F, Roncarolo MG, Behrens TW, Grillot DA, Nunez G, Lees E, Howard M |
| المصدر: | The Journal of experimental medicine [J Exp Med] 1998 Apr 06; Vol. 187 (7), pp. 1081-91. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Rockefeller University Press Country of Publication: United States NLM ID: 2985109R Publication Model: Print Cited Medium: Print ISSN: 0022-1007 (Print) Linking ISSN: 00221007 NLM ISO Abbreviation: J Exp Med Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: New York, NY : Rockefeller University Press |
| مواضيع طبية MeSH: | B-Lymphocytes/*metabolism , Gene Expression Regulation/*genetics , Immunoglobulins/*immunology , Mice, Transgenic/*immunology , Proto-Oncogene Proteins c-bcl-2/*genetics, Agammaglobulinaemia Tyrosine Kinase ; Animals ; Antigens, CD/immunology ; Apoptosis/physiology ; Bromodeoxyuridine/metabolism ; Cell Count ; Cell Cycle/physiology ; Cell Survival ; Disease Models, Animal ; Flow Cytometry ; Mice ; Mice, Inbred CBA ; Phenotype ; Protein Kinases/analysis ; Protein-Tyrosine Kinases/genetics ; Proto-Oncogene Proteins c-bcl-2/analysis ; Spleen/cytology ; bcl-X Protein |
| مستخلص: | Mutations in the tyrosine kinase, Btk, result in a mild immunodeficiency in mice (xid). While B lymphocytes from xid mice do not proliferate to anti-immunoglobulin (Ig), we show here induction of the complete complement of cell cycle regulatory molecules, though the level of induction is about half that detected in normal B cells. Cell cycle analysis reveals that anti-Ig stimulated xid B cells enter S phase, but fail to complete the cell cycle, exhibiting a high rate of apoptosis. This correlated with a decreased ability to induce the anti-apoptosis regulatory protein, Bcl-xL. Ectopic expression of Bcl-xL in xid B cells permitted anti-Ig induced cell cycle progression demonstrating dual requirements for induction of anti-apoptotic proteins plus cell cycle regulatory proteins during antigen receptor mediated proliferation. Furthermore, our results link one of the immunodeficient traits caused by mutant Btk with the failure to properly regulate Bcl-xL. |
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| المشرفين على المادة: | 0 (Antigens, CD) 0 (Bcl2l1 protein, mouse) 0 (Immunoglobulins) 0 (Proto-Oncogene Proteins c-bcl-2) 0 (bcl-X Protein) EC 2.7.- (Protein Kinases) EC 2.7.10.1 (Protein-Tyrosine Kinases) EC 2.7.10.2 (Agammaglobulinaemia Tyrosine Kinase) EC 2.7.10.2 (Btk protein, mouse) G34N38R2N1 (Bromodeoxyuridine) |
| تواريخ الأحداث: | Date Created: 19980516 Date Completed: 19980508 Latest Revision: 20231105 |
| رمز التحديث: | 20231105 |
| مُعرف محوري في PubMed: | PMC2212200 |
| DOI: | 10.1084/jem.187.7.1081 |
| PMID: | 9529324 |
| قاعدة البيانات: | MEDLINE |
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