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STING couples with PI3K to regulate actin reorganization during BCR activation.

Science advances (2020-06-05)
Yukai Jing, Xin Dai, Lu Yang, Danqing Kang, Panpan Jiang, Na Li, Jiali Cheng, Jingwen Li, Heather Miller, Boxu Ren, Quan Gong, Wei Yin, Zheng Liu, Pieta K Mattila, Qin Ning, Jinqiao Sun, Bing Yu, Chaohong Liu
ZUSAMMENFASSUNG

The adaptor protein, STING (stimulator of interferon genes), has been rarely studied in adaptive immunity. We used Sting KO mice and a patient's mutated STING cells to study the effect of STING deficiency on B cell development, differentiation, and BCR signaling. We found that STING deficiency promotes the differentiation of marginal zone B cells. STING is involved in BCR activation and negatively regulates the activation of CD19 and Btk but positively regulates the activation of SHIP. The activation of WASP and accumulation of F-actin were enhanced in Sting KO B cells upon BCR stimulation. Mechanistically, STING uses PI3K mediated by the CD19-Btk axis as a central hub for controlling the actin remodeling that, in turn, offers feedback to BCR signaling. Overall, our study provides a mechanism of how STING regulates BCR signaling via feedback from actin reorganization, which contributes to positive regulation of STING on the humoral immune response.

MATERIALIEN
Produktnummer
Marke
Produktbeschreibung

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PMA, for use in molecular biology applications, ≥99% (HPLC)
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Sigma Adjuvant System®, oil
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Saponin Quillaja sp., Sapogenin content 20-35 %
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Anti-Phosphotyrosin-Antikörper, Klon 4G10®, clone 4G10®, Upstate®, from mouse
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DL-Cystein, technical grade
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PI 3-Kδ-Inhibitor X, IC87114, The PI 3-Kδ Inhibitor X, IC87114, also referenced under CAS 371242-69-2, controls the biological activity of PI 3-Kδ. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.