Present specialized field
（Last updated : 2021-09-21 08:12:32）
Present specialized field
SH3BP2 Deficiency Ameliorates Murine Systemic Lupus Erythematosus.
Functional analysis of a novel G87V TNFRSF1A mutation in patients with TNF receptor-associated periodic syndrome
IL-6-PAD4 axis in the earliest phase of arthritis in knock-in gp130F759 mice, a model for rheumatoid arthritis
Sh3bp2 Gain-Of-Function Mutation Ameliorates Lupus Phenotypes in B6.MRL-Faslpr Mice.
Cyclosporin A indirectly attenuates activation of group 2 innate lymphoid cells in papain-induced lung inflammation.
controls the production and function of dendritic cells and regulates the induction of IFN-gamma-producing T cells.
Lnk prevents inflammatory CD8
T-cell proliferation and contributes to intestinal homeostasis.
TWEAK/Fn14 pathway promotes a T helper 2-type chronic colitis with fibrosis in mice.
Thymic stromal lymphopoietin (TSLP)-induced polyclonal B-cell activation and autoimmunity are mediated by CD4
T cells and IL-4.
Dibutyl phthalate-induced thymic stromal lymphopoietin is required for Th2 contact hypersensitivity responses.
Cutting edge: Inhibition of NF-kappaB-mediated TSLP expression by retinoid X receptor.
Local increase in thymic stromal lymphopoietin induces systemic alterations in B cell development.
Differential Role of SH2-B and APS in Regulating Energy and Glucose Homeostasis
Enhanced engraftment of hematopoietic stem/progenitor cells by the transient inhibition of an adaptor protein, Lnk.
APS, an adaptor molecule containing PH and SH2 domains, has a negative regulatory role in B cell proliferation.
Increased numbers of B-1 cells and enhanced responses against TI-2 antigen in mice lacking APS, an adaptor molecule containing PH and SH2 domains.
Roles of a conserved family of adaptor proteins, Lnk, SH2-B, and APS, for mast cell development, growth, and functions: APS-deficiency causes augmented degranulation and reduced actin assembly
Increased insulin sensitivity and hypoinsulinemia in APS knockout mice.
SH2-B is required for both male and female reproduction.
Molecular Cloning of the Mouse APS as a Member of the Lnk Family Adaptor Proteins
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Lack of bone marrow stromal cell antigen-1 (BST-1)/CD157 ameliorated colitis induced by dextran sodium sulfate (DSS)
BST-1/CD157 promotes epithelial damages in DSS-induced colitis.
Lack of BST-1/CD157 ameliorated fibroblastic changes of arthritis in GP130F759 through down regulation of IL-6 production by synovial fibroblasts.
The role of an adaptor protein SH3BP2 in the pathogenesis of systemic lupus erythematosus
SH3BP2 Deciency Ameliorates Murine Systemic Lupus Erythematosus
SH3BP2 deficiency ameliorates murine systemic lupus erythematosus
IL-6-PAD4 axis in the preclinical state of the synovium in gp130F759
-interaction between fibroblast-like synoviocytes and neutrophils-
IL-6-PAD4 axis: IL-6 dependent PAD4 production in neutrophils at the earliest phase of arthritis in gp130F759.
Toll-like receptor-induced Ab production from marginal zone B cells is negatively regulated by ADP-ribosyl cyclase BST-1/CD157
The role of adopter protein SH3BP2 in a murine systemic lupus erythematosus model
The Study of the Novel G87V Mutation in the TNFRSF1A Gene Identified in a Family with TNF Receptor-Associated Periodic Syndrome (TRAPS)
macrophage-like synoviocytes in gp130F759, a mouse model for rheumatoid arthritis
SH3BP2 gain-of-function mutation ameliorates lupus in B6.MRL-Faslpr mice
The Study of the novel G58V mutation in the TNFRSF1A gene identified in a family with TNF Receptor-Associated Periodic Syndrome(TRAPS)
BST-1/CD157 negatively regulates marginal zone B cell survival and Ab production induced with Toll-like receptor stimulation
exacerbated the arthritis in gp130F759.
Elongation of the small intestine and enlargement of the mesenteric lymph nodes in Bst1Cd38 double knockout mice.
The novel G58V mutation in the TNFRSF1A gene identified in a family with TNF Receptor-Associated Periodic Syndrome (TRAPS) decreases the cell surface expression of TNFR1
A novel function of ADP-ribosyl cyclases to regulate the length of the small intestine revealed in CD38/CD157 double knockout mice
Accelerated onset of arthritis by systemic infection of Mycoplasma fermentans in the knock-in mice gp130F759
SH3BP2 gain-of-function mutation alleviates lupus phenotypes in B6.MRL-Faslpr mice
Functional analysis of the novel G58V mutation in the TNFRSF1A gene identified in a family with TNF receptor-associated periodic syndrome(TRAPS)
BST-1/CD157 on B cells negatively regulates Toll-like receptor signaling
SH3BP2 Gain-of-Function Mutation Ameliorates Lupus in B6.MRL-Faslpr Mice
Functional Analysis of the Novel G58V Mutation in the TNFRSF1A Gene Identified in a Family with TNF Receptor-Associated Periodic Syndrome (TRAPS)
Lack of microbiota revealed the role for BST-1/CD157 to maintain the homeostasis at mucosa-MLN interface
Germinal center B cell survival and optimal IgE production are controled by Lnk/Sh2b family adaptor protein Aps/Sh2b2.
Lnk/Sh2b family adaptor protein Aps/Sh2b2 in B cells contributes to germinal center B cell survival and optimal IgE production
Lnk/Sh2b3 adaptor protein controls cytokine responses of dendritic cells, and regulates the induction of IFN-gamma-producing T cells.
IgE production and germinal center formation are regulated by the adaptor protein Aps/Sh2b2 in B cells.
An autoimmune disease-associated gene, Lnk/SH2B3 controls production and functions of DC subsets and regulates inflammatory T cell differentiation.
Lnk/Sh2b3 adaptor protein prevents the accumulation of inflammatory CD8+ T cells and intestinal villous atrophy.
Lnk/Sh2b3, and intracellular adaptor associated with celiac disease and autoimmune diabetes, regulates accumulation of inflammatory T cells and prevents intestinal villous atrophy.
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The Japanese Society for Immunology (JSI)
The Molecular Biology Society of Japan (MBSJ)
Japan College of Rheumatology
© 2008 Kawasaki Medical School