ACKR3 蛋白, Human (His-SUMO)

ACKR3, an atypical chemokine receptor, precisely controls chemokine levels and localization through high-affinity binding, operating independently of ligand-driven signal transduction. It serves as an interceptor, internalizing receptor, and chemokine-scavenger for CXCL11 and CXCL12/SDF1, inducing beta-arrestin recruitment, ligand internalization, and MAPK pathway activation. Essential for regulating CXCR4 in interneurons and promoting survival in glioma cells, ACKR3 also influences malignant hematopoietic cell adhesion and migration. Its regulatory roles extend to heart valve development, axon guidance, and HIV infection collaboration with CXCR4. ACKR3 Protein, Human (His-SUMO) is the recombinant human-derived ACKR3 protein, expressed by E. coli, with N-SUMO, N-6*His labeled tag. The total length of ACKR3 Protein, Human (His-SUMO) is 40 a.a., with molecular weight of 20.5 kDa.

ACKR3 是一种非典型趋化因子受体，通过高亲和力趋化因子结合对趋化因子水平和定位进行精确控制，其运作独立于传统配体驱动的信号转导级联。作为拦截器、内化受体、趋化因子清除受体或趋化因子诱饵受体，ACKR3 与 CXCL11 和 CXCL12/SDF1 等趋化因子结合，而不激活 G 蛋白介导的信号转导。相反，趋化因子结合会诱导 β-抑制蛋白募集，导致配体内化和 MAPK 信号通路激活。在迁移的中间神经元中，ACKR3 对于调节 CXCR4 蛋白水平、调整其对趋化因子的反应至关重要。在神经胶质瘤细胞中，ACKR3 通过 MEK/ERK 途径转导信号，赋予细胞凋亡抵抗力并促进细胞生长和存活。虽然不影响正常造血祖细胞的迁移、粘附或增殖，但当恶性造血细胞中的 CXCL11 激活时，ACKR3 会通过 ERK1/2 磷酸化增强细胞粘附和迁移。此外，ACKR3 在 CXCR4 介导的细胞表面整合素激活中发挥调节作用，对心脏瓣膜发育至关重要。在动眼神经系统中，ACKR3 通过调节 CXCL12 水平来调节轴突引导。此外，作为 CXCR4 的共受体，ACKR3 在微生物感染期间与有限数量的 HIV 分离株合作。

Human

E. coli

N-SUMO;N-6*His

P25106 (M1-K40)

57007  [NCBI]

MDLHLFDYSEPGNFSDISWPCNSSDCIVVDTVMCPNMPNK

20.5 kDa

Greater than 90% as determined by reducing SDS-PAGE.

<1 EU/μg, determined by LAL method.