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Functional receptors on B-cell membranesCampbell, M-A. January 1988 (has links)
No description available.
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Identification of the cellular factors that regulate expression of the Epstein-Barr virus BZLF1 gene in differentiating human epithelial cellsMacCallum, Paul Robert January 2001 (has links)
No description available.
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Differential roles of ERK-MAPKinase in WEHI-231 cell apoptosis and growthGauld, Stephen Baxter January 2000 (has links)
No description available.
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The Role of Homeodomain-interacting Protein Kinase (HIPK)-1 in B LymphocytesGuerra, Fiona 30 August 2011 (has links)
The homeodomain-interacting protein kinase (HIPK) family is comprised of four evolutionarily conserved and highly related serine/threonine kinases originally identified as co-repressors for homeodomain-containing transcription factors. While the HIPKs are most noted for regulation of apoptosis, proliferation and differentiation, I report a pleiotropic function of HIPK1 within the B cell lineage. Although lymphocyte development was normal within the thymus and bone marrow of HIPK1-deficient (HIPK1-/-) mice, the spleen exhibited a reduced number of transitional and follicular (FO) B cells, but with an increase in the marginal zone (MZ) B cell population. HIPK1-/- B cells exhibited impaired proliferation in response to B cell receptor (BCR) cross-linking in vitro; and immunization of HIPK1-/- mice with T-independent type 2 (TI-2) antigen resulted in a significantly impaired humoral response despite the expanded MZ B cell population. Immunization with T-dependent (TD) antigen resulted in a kinetically delayed response, with impaired affinity maturation. Identification of a kinase-substrate interaction between HIPK1 and the B cell adaptor 3BP2 suggests a potential context for HIPK1 function in BCR signaling. HIPK1-/- B cells were uniquely resistant to reactive oxygen species (ROS)-induced apoptosis, but equally susceptible to UV- and γ-irradiation compared to controls. In vitro class-switch recombination (CSR) assays revealed that HIPK1 is required for the negative regulation of CSR. HIPK1-/- B cell cultures harbored more viable cells, more switched cells, and elevated AID mRNA levels. The findings presented in this thesis demonstrate that HIPK1 is required for splenic B cell homeostasis and optimal BCR-responsiveness. In contrast, HIPK1 is also required for the negative regulation of CSR, possibly by mediating CSR-induced apoptosis.
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The Role of Homeodomain-interacting Protein Kinase (HIPK)-1 in B LymphocytesGuerra, Fiona 30 August 2011 (has links)
The homeodomain-interacting protein kinase (HIPK) family is comprised of four evolutionarily conserved and highly related serine/threonine kinases originally identified as co-repressors for homeodomain-containing transcription factors. While the HIPKs are most noted for regulation of apoptosis, proliferation and differentiation, I report a pleiotropic function of HIPK1 within the B cell lineage. Although lymphocyte development was normal within the thymus and bone marrow of HIPK1-deficient (HIPK1-/-) mice, the spleen exhibited a reduced number of transitional and follicular (FO) B cells, but with an increase in the marginal zone (MZ) B cell population. HIPK1-/- B cells exhibited impaired proliferation in response to B cell receptor (BCR) cross-linking in vitro; and immunization of HIPK1-/- mice with T-independent type 2 (TI-2) antigen resulted in a significantly impaired humoral response despite the expanded MZ B cell population. Immunization with T-dependent (TD) antigen resulted in a kinetically delayed response, with impaired affinity maturation. Identification of a kinase-substrate interaction between HIPK1 and the B cell adaptor 3BP2 suggests a potential context for HIPK1 function in BCR signaling. HIPK1-/- B cells were uniquely resistant to reactive oxygen species (ROS)-induced apoptosis, but equally susceptible to UV- and γ-irradiation compared to controls. In vitro class-switch recombination (CSR) assays revealed that HIPK1 is required for the negative regulation of CSR. HIPK1-/- B cell cultures harbored more viable cells, more switched cells, and elevated AID mRNA levels. The findings presented in this thesis demonstrate that HIPK1 is required for splenic B cell homeostasis and optimal BCR-responsiveness. In contrast, HIPK1 is also required for the negative regulation of CSR, possibly by mediating CSR-induced apoptosis.
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Histologic identification of immunologically induced B-lymphocytesChinea, José J. January 1973 (has links)
This document only includes an excerpt of the corresponding thesis or dissertation. To request a digital scan of the full text, please contact the Ruth Lilly Medical Library's Interlibrary Loan Department (rlmlill@iu.edu).
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Cross-talk between marginal zone B cells and marginal zone macrophagesYou, Yuying. January 2010 (has links) (PDF)
Thesis (Ph.D.)--University of Alabama at Birmingham, 2010. / Title from PDF title page (viewed on July 8, 2010). Includes bibliographical references.
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IgE production regulation via CD23 stalk engagement and cell cycle stimulation /Caven, Timothy Hays, January 2006 (has links)
Thesis (Ph. D.)--Virginia Commonwealth University, 2006. / Prepared for: Dept. of Microbiology and Immunology. Includes bibliographical references (p. 210-222). Also available online.
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A mathematical model of steady state B lymphopoiesis in mouse and rat bone marrow /Karanfil, Özge. January 2007 (has links)
No description available.
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A mathematical model of steady state B lymphopoiesis in mouse and rat bone marrow /Karanfil, Özge. January 2007 (has links)
In this study, we have analyzed the steady-state kinetics of B lymphocytes in mouse and rat bone marrow using previously published experimental data. Over many years, Prof D.G. Osmond and his colleagues have built up a scheme of B cell development in mouse bone marrow based on the sequential expression of markers associated with the B lineage. The earliest precursor B cells comprise three populations of proliferating pro-B cells, i.e. early, intermediate, and late pro-B cells. The subsequent populations comprise pre-B cells that give rise to nondividing B lymphocytes expressing surface IgM. / In our analysis, we have checked the available published data for consistency with the proliferation of precursor B cells and their death via apoptosis at certain stages of cell development. We made an extensive summary of the existing data on the various B cell precursors and organized it into a comprehensible framework. We built a mathematical model for the proliferation and differentiation of mammalian B lymphocytes in laboratory mice and rats and estimated all of the parameters to explain the existing steady state data. In this context, mathematical modeling acts as a useful tool to analyze hypotheses and experimental results concerning the steady state numbers of B lymphocytes.
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