2010年5月14日 · Spleen tyrosine kinase (SYK) is a non-receptor tyrosine kinase that has long been thought to exclusively mediate signalling by receptors of the adaptive immune response...

BCR 聚集后快速激活 Src 家族激酶 Lyn、Blk 和 Fyn，以及酪氨酸激酶 Syk 和 Btk。 这就启动形成一个由 BCR 组成的“信号小体” 、上述酪氨酸激酶、 连接蛋白（如 CD19 和 BLNK），以及信号转导酶，如 PLCγ2、PI3K 和 Vav。

Syk是BCR信号通路的关键激酶，含有两个SH2结构域，正好识别ITAM上的两个pTyr，能识别并磷酸化下游的多种蛋白，同时自身也能被磷酸化。 CD19/CD21/CD81复合物又被称为B细胞辅助受体（B cell co-receptor），功能和T细胞的CD4/CD8类似。

In this study, we first demonstrate that CD40 ligation modifies BCR-induced B cell activation by promoting activation of Syk and formation of signaling complex consisting of Syk, Vav-2, Btk, BLNK, and PLC-γ2, thus leading to activation of p38 MAPK, ERK, Akt, and NF-κB.

2021年3月29日 · Spleen tyrosine kinase (SYK) is one of the proteins necessary for the proper development and function of B cells. SYK has a role in transmitting signals from the...

在B细胞中，BCR激活后将ITAM暴露给LYN/SYK/BTK，进而激活PLCγ2和 磷脂酰肌醇3-激酶 (PI3K)。 活化的PLCγ2和PI3K进而激活钙离子介导的信号通路，从而激活下游的转录因子，例如NFAT和NF-κB，这些信号通路能够调节细胞增殖、存活和细胞因子表达。 有几种BTK抑制剂已经进入了临床研究，在治疗复发性多发性硬化症的临床II期研究中，Evobrutinib在使用3个月后能够减小脑损伤斑块。 Branebrutinib（BMS-986195）已进入到治疗类风湿性关节炎、 干燥综合征 …

2025年1月1日 · SYK, a key signal transducer downstream of the BCR, is considered one of the most promising targets for SLE. SYK phosphorylation was decreased after BCR activation in patients with SLE. (p57), (p58) TLR9 expression activates TRAF6 through the MyD88-mediated signaling pathway, which in turn affects the immune response and inflammatory processes.

2008年2月15日 · Ligand-induced BCR signaling induces receptor oligomerization, Igalpha/beta immunoreceptor tyrosine-based activation motif (ITAM) phosphorylation, and activation of the spleen tyrosine kinase (SYK), which initiates downstream events and amplifies the …

2008年12月18日 · We now report that Syk is constitutively phosphorylated on the activating Y352 residue in chronic lymphocytic leukemia (CLL) B cells. To examine the effects of constitutive Syk activity on...

2013年6月10日 · In this study, we characterize distinct SYK/PI3K/AKT-dependent BCR viability pathways in DLBCL cell lines and primary tumors with high- and low-baseline NF-κB activity and define SYK/PI3K/AKT-dependent repression of the pro-apoptotic HRK protein as an important survival mechanism in BCR-dependent NF-κB low DLBCLs (Figure 8A).