Tyrosine phosphorylation of 3BP2 is indispensable for the interaction with VAV3 in chicken DT40 cells

Chihara, Kazuyasu; Kimura, Yukihiro; Honjoh, Chisato; Yamauchi, Shota; Takeuchi, Kenji; Sada, Kiyonao

doi:10.1016/j.yexcr.2013.12.026

Cited by 11 publications

(16 citation statements)

References 32 publications

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“…It has been reported that SH3BP2 plays roles in T-cell [18], [56] and B-cell responses [14], [15], [57]–[59]. However, SH3BP2 gain-of-function mutation did not alter the T- and B-cell responses in the CIA model (Figure 6).…”

Section: Discussionmentioning

confidence: 83%

SH3BP2 Gain-Of-Function Mutation Exacerbates Inflammation and Bone Loss in a Murine Collagen-Induced Arthritis Model

et al. 2014

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ObjectiveSH3BP2 is a signaling adapter protein which regulates immune and skeletal systems. Gain-of-function mutations in SH3BP2 cause cherubism, characterized by jawbone destruction. This study was aimed to examine the role of SH3BP2 in inflammatory bone loss using a collagen-induced arthritis (CIA) model.MethodsCIA was induced in wild-type (Sh3bp2+/+) and heterozygous P416R SH3BP2 cherubism mutant knock-in (Sh3bp2KI/+) mice, an SH3BP2 gain-of-function model. Severity of the arthritis was determined by assessing the paw swelling and histological analyses of the joints. Micro-CT analysis was used to determine the levels of bone loss. Inflammation and osteoclastogenesis in the joints were evaluated by quantitating the gene expression of inflammatory cytokines and osteoclast markers. Furthermore, involvement of the T- and B-cell responses was determined by draining lymph node cell culture and measurement of the serum anti-mouse type II collagen antibody levels, respectively. Finally, roles of the SH3BP2 mutation in macrophage activation and osteoclastogenesis were determined by evaluating the TNF-α production levels and osteoclast formation in bone marrow-derived M-CSF-dependent macrophage (BMM) cultures.Results Sh3bp2KI/+ mice exhibited more severe inflammation and bone loss, accompanying an increased number of osteoclasts. The mRNA levels for TNF-α and osteoclast marker genes were higher in the joints of Sh3bp2KI/+ mice. Lymph node cell culture showed that lymphocyte proliferation and IFN-γ and IL-17 production were comparable between Sh3bp2+/+ and Sh3bp2KI/+ cells. Serum anti-type II collagen antibody levels were comparable between Sh3bp2+/+ and Sh3bp2KI/+ mice. In vitro experiments showed that TNF-α production in Sh3bp2KI/+ BMMs is elevated compared with Sh3bp2+/+ BMMs and that RANKL-induced osteoclastogenesis is enhanced in Sh3bp2KI/+ BMMs associated with increased NFATc1 nuclear localization.ConclusionGain-of-function of SH3BP2 augments inflammation and bone loss in the CIA model through increased macrophage activation and osteoclast formation. Therefore, modulation of the SH3BP2 expression may have therapeutic potential for the treatment of rheumatoid arthritis.

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Section: Discussionmentioning

confidence: 83%

SH3BP2 Gain-Of-Function Mutation Exacerbates Inflammation and Bone Loss in a Murine Collagen-Induced Arthritis Model

et al. 2014

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“…After the stimulation, cells were washed with ice-cold PBS twice and solubilized in the lysis buffer (50 mM Tris, pH 7.4, 150 mM NaCl, 10 mM EDTA, 100 mM NaF, 1 mM Na 3 VO 4 , 1 mM PMSF, and 2 g/ml aprotinin) containing 1% Triton X-100. Preparation of detergentsoluble cell lysates, immunoprecipitation, and immunoblotting were performed as described previously (32)(33)(34). Pull-down Assay-The GST-rat Syk-SH2 (both N-and C-terminal SH2 domains) expression construct was a gift from Dr. Reuben P. Siraganian.…”

Section: Methodsmentioning

confidence: 99%

“…5 ϫ 10 6 cells were incubated without or with 100 g/ml curdlan in medium and were solubilized with the lysis buffer containing 1% Triton X-100. In vitro binding experiments were performed as described previously (32)(33)(34).…”

Section: Methodsmentioning

confidence: 99%

Dectin-1-mediated Signaling Leads to Characteristic Gene Expressions and Cytokine Secretion via Spleen Tyrosine Kinase (Syk) in Rat Mast Cells

Kimura

Chihara

Honjoh

et al. 2014

Journal of Biological Chemistry

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Background: ␤-Glucan receptor Dectin-1 in dendritic cells and macrophages plays important roles in antifungal immunity. Results: Dectin-1 is expressed in rat mast cells, and its tyrosine phosphorylation induces characteristic gene expression of transcription factors and cytokines through protein-tyrosine kinase Syk. Conclusion: Dectin-1 functions in rat mast cells. Significance: Dectin-1-mediated signaling in mast cells may contribute to antifungal immunity.

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“…In some experiments, Syk inhibitors (R406 and BAY61-3606) were added to the culture medium before stimulation. Preparation of cell lysates and immunoprecipitation were performed as described previously165657585960.…”

Section: Methodsmentioning

confidence: 99%

“…Proteins were visualized using enhanced chemiluminesence reagent (Western Lightning Plus-ECL, Perkin Elmer Life Sciences, Waltham, MA). The antibodies bound to membrane were stripped and reprobed with the other antibodies as described165657585960.…”

Section: Methodsmentioning

confidence: 99%

Association of C-Type Lectin Mincle with FcεRIβγ Subunits Leads to Functional Activation of RBL-2H3 Cells through Syk

Honjoh

Chihara

Yoshiki

et al. 2017

Sci Rep

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Macrophage-inducible C-type lectin (Mincle) interacts with the γ-subunit of high-affinity IgE receptor (FcεRIγ) and activates Syk by recognizing its specific ligand, trehalose-6,6′-dimycolate, a glycolipid produced by Mycobacterium tuberculosis. It has been suggested that mast cells participate in the immune defense against pathogenic microbes including M. tuberculosis, although the functions are still uncertain. In this study, we examined the Mincle-mediated signaling pathway and cellular responses using RBL-2H3 cells. Mincle formed a protein complex with not only FcεRIγ but also FcεRIβ in a stable cell line expressing myc-tagged Mincle. In addition, engagement of Mincle increased the levels of protein tyrosine phosphorylation and ERK phosphorylation. A pull-down assay demonstrated that cross-linking of Mincle induced binding of FcεRIβγ subunits to the Src homology 2 domain of Syk. Pharmacological and genetic studies indicated that activation of Syk was critical for Mincle-mediated activation of phospholipase Cγ2, leading to the activation of ERK and nuclear factor of activated T cells. Moreover, engagement of Mincle efficiently induced up-regulation of characteristic mast cell genes in addition to degranulation. Taken together, our present results suggest that mast cells contribute to Mincle-mediated immunity through Syk activation triggered by association with the FcεRIβγ complex.

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Tyrosine phosphorylation of 3BP2 is indispensable for the interaction with VAV3 in chicken DT40 cells

Cited by 11 publications

References 32 publications

SH3BP2 Gain-Of-Function Mutation Exacerbates Inflammation and Bone Loss in a Murine Collagen-Induced Arthritis Model

SH3BP2 Gain-Of-Function Mutation Exacerbates Inflammation and Bone Loss in a Murine Collagen-Induced Arthritis Model

Dectin-1-mediated Signaling Leads to Characteristic Gene Expressions and Cytokine Secretion via Spleen Tyrosine Kinase (Syk) in Rat Mast Cells

Association of C-Type Lectin Mincle with FcεRIβγ Subunits Leads to Functional Activation of RBL-2H3 Cells through Syk

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