Systemic ST6Gal-1 Is a Pro-survival Factor for Murine Transitional B Cells
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Title
Systemic ST6Gal-1 Is a Pro-survival Factor for Murine Transitional B Cells
Authors
Keywords
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Journal
Frontiers in Immunology
Volume 9, Issue -, Pages -
Publisher
Frontiers Media SA
Online
2018-09-20
DOI
10.3389/fimmu.2018.02150
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- (2017) Fernando Spiller et al. JOURNAL OF IMMUNOLOGY
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- (2016) Matthew J. Schultz et al. CANCER RESEARCH
- B-cell–independent sialylation of IgG
- (2016) Mark B. Jones et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- APOBEC3 enzymes restrict marginal zone B cells
- (2015) Gabriele B. Beck-Engeser et al. EUROPEAN JOURNAL OF IMMUNOLOGY
- Siglec-G Deficiency Leads to Autoimmunity in Aging C57BL/6 Mice
- (2015) Jennifer Müller et al. JOURNAL OF IMMUNOLOGY
- BAFF promotes proliferation of human mesangial cells through interaction with BAFF-R
- (2015) Nuoyan Zheng et al. BMC Nephrology
- Siglec-G/10 in self-nonself discrimination of innate and adaptive immunity
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- Remodeling of Marrow Hematopoietic Stem and Progenitor Cells by Non-self ST6Gal-1 Sialyltransferase
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- Siglecs Induce Tolerance to Cell Surface Antigens by BIM-Dependent Deletion of the Antigen-Reactive B Cells
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- Copresentation of Antigen and Ligands of Siglec-G Induces B Cell Tolerance Independent of CD22
- (2013) F. Pfrengle et al. JOURNAL OF IMMUNOLOGY
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- (2013) Allison Sang et al. MOLECULAR IMMUNOLOGY
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- (2012) Yadira Ledesma-Soto et al. BMC IMMUNOLOGY
- Anti-inflammatory IgG Production Requires Functional P1 Promoter in β-Galactoside α2,6-Sialyltransferase 1 (ST6Gal-1) Gene
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- Signaling by the tumor necrosis factor receptor superfamily in B-cell biology and disease
- (2011) Robert C. Rickert et al. IMMUNOLOGICAL REVIEWS
- Sialylation of the Fas Death Receptor by ST6Gal-I Provides Protection against Fas-mediated Apoptosis in Colon Carcinoma Cells
- (2011) Amanda F. Swindall et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- BAFF Receptor Signaling Aids the Differentiation of Immature B Cells into Transitional B Cells following Tonic BCR Signaling
- (2010) S. L. Rowland et al. JOURNAL OF IMMUNOLOGY
- Augmented B Lymphocyte Response to Antigen in the Absence of Antigen-Induced B Lymphocyte Signaling in an IgG-Transgenic Mouse Line
- (2010) Rong-Yong Man et al. PLoS One
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- (2009) W. N. Khan JOURNAL OF IMMUNOLOGY
- Altered eosinophil profile in mice with ST6Gal-1 deficiency: an additional role for ST6Gal-1 generated by the P1 promoter in regulating allergic inflammation
- (2009) M. Nasirikenari et al. JOURNAL OF LEUKOCYTE BIOLOGY
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- (2008) Daniel R Christie et al. Journal of Ovarian Research
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