Ablation of CD22 in ligand-deficient mice restores B cell receptor signaling. - Wikidata - wikimedia - TriplyDB

Ablation of CD22 in ligand-deficient mice restores B cell receptor signaling.

Ablation of CD22 in ligand-deficient mice restores B cell receptor signaling.

http://www.wikidata.org/entity/Q46963835

about

Siglecs as sensors of self in innate and adaptive immune responses Siglecs and immune regulation Infection, inflammation and host carbohydrates: a Glyco-Evasion Hypothesis Rethinking mechanisms of autoimmune pathogenesis CD22: an inhibitory enigma B cell antigen receptor signal strength and peripheral B cell development are regulated by a 9-O-acetyl sialic acid esterase Molecular phylogeny and functional genomics of beta-galactoside alpha2,6-sialyltransferases that explain ubiquitous expression of st6gal1 gene in amniotes.Decoration of T-independent antigen with ligands for CD22 and Siglec-G can suppress immunity and induce B cell tolerance in vivo Alpha2,6-sialic acid on platelet endothelial cell adhesion molecule (PECAM) regulates its homophilic interactions and downstream antiapoptotic signaling.Altered eosinophil profile in mice with ST6Gal-1 deficiency: an additional role for ST6Gal-1 generated by the P1 promoter in regulating allergic inflammation.In situ trans ligands of CD22 identified by glycan-protein photocross-linking-enabled proteomics.Role for hepatic and circulatory ST6Gal-1 sialyltransferase in regulating myelopoiesis.Siglec-mediated regulation of immune cell function in disease.Emerging role of alpha2,6-sialic acid as a negative regulator of galectin binding and function.ST6Gal-I restrains CD22-dependent antigen receptor endocytosis and Shp-1 recruitment in normal and pathogenic immune signaling Characterizing the glycome of the mammalian immune system.Sialylated multivalent antigens engage CD22 in trans and inhibit B cell activation.Treatment response in Kawasaki disease is associated with sialylation levels of endogenous but not therapeutic intravenous immunoglobulin G Distinct endocytic mechanisms of CD22 (Siglec-2) and Siglec-F reflect roles in cell signaling and innate immunity.Nanoscale organization and dynamics of the siglec CD22 cooperate with the cytoskeleton in restraining BCR signalling.Sialic acids and autoimmune disease.CD22 ligand-binding and signaling domains reciprocally regulate B-cell Ca2+ signaling.B-cell-independent sialylation of IgG.The generation of influenza-specific humoral responses is impaired in ST6Gal I-deficient mice N-Glycans in cancer progression.Regulation of B-cell entry into the cell cycle Glycopolymer probes of signal transduction Mammalian glycosylation in immunity.Dendritic cell-dependent inhibition of B cell proliferation requires CD22 Basic and clinical immunology of Siglecs Siglecs as targets for therapy in immune-cell-mediated disease.Esterases and autoimmunity: the sialic acid acetylesterase pathway and the regulation of peripheral B cell tolerance.Adaptive immune activation: glycosylation does matter.Liver membrane proteome glycosylation changes in mice bearing an extra-hepatic tumor.CD22 and autoimmune disease.Increasing the α 2, 6 sialylation of glycoproteins may contribute to metastatic spread and therapeutic resistance in colorectal cancer.CD22 and Siglec-G regulate inhibition of B-cell signaling by sialic acid ligand binding and control B-cell tolerance.Bifunctional CD22 ligands use multimeric immunoglobulins as protein scaffolds in assembly of immune complexes on B cells.Sialylation of N-glycans: mechanism, cellular compartmentalization and function.DropArray™, a wall-less 96-well plate for uptake and immunofluorescence microscopy, confirms CD22 recycles.

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P2860

Ablation of CD22 in ligand-deficient mice restores B cell receptor signaling.

http://www.wikidata.org/entity/Q46963835

description

2005 nî lūn-bûn

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name

Ablation of CD22 in ligand-deficient mice restores B cell receptor signaling.

@en

Ablation of CD22 in ligand-deficient mice restores B cell receptor signaling.

@nl

type

label

Ablation of CD22 in ligand-deficient mice restores B cell receptor signaling.

@en

Ablation of CD22 in ligand-deficient mice restores B cell receptor signaling.

@nl

prefLabel

Ablation of CD22 in ligand-deficient mice restores B cell receptor signaling.

@en

Ablation of CD22 in ligand-deficient mice restores B cell receptor signaling.

@nl

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Nature Immunology

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Ablation of CD22 in ligand-deficient mice restores B cell receptor signaling.

@en

P2093

Brian A Smith

http://www.w3.org/2001/XMLSchema#string

Brian E Collins

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James C Paulson

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Per Bengtson

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P2860

B cell signaling. Introduction

Inhibition of the B cell by CD22: a requirement for Lyn

Siglecs in the immune system

Polygenic autoimmune traits: Lyn, CD22, and SHP-1 are limiting elements of a biochemical pathway regulating BCR signaling and selection

Molecular interactions regulate BCR signal inhibition by CD22 and CD72

Sialoadhesin, myelin-associated glycoprotein and CD22 define a new family of sialic acid-dependent adhesion molecules of the immunoglobulin superfamily

Definition of the sites of interaction between the protein tyrosine phosphatase SHP-1 and CD22

CD22 is a negative regulator of B-cell receptor signalling

Hyperresponsive B cells in CD22-deficient mice

Sialic acid binding domains of CD22 are required for negative regulation of B cell receptor signaling

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