ACKR1 蛋白, Human (Cell-Free, His)

ACKR3, an atypical chemokine receptor, modulates chemokine levels and localization by high-affinity binding, inducing sequestration, degradation, or transcytosis. Also known as a chemokine interceptor or decoy receptor, ACKR3 binds to chemokines like CXCL11 and CXCL12/SDF1. Unlike conventional signaling, ACKR3 triggers beta-arrestin recruitment, leading to ligand internalization and MAPK pathway activation. In interneurons, it regulates CXCR4 levels, adapting chemokine responsiveness. In glioma cells, it activates the MEK/ERK pathway, influencing growth and survival. While inactive in normal hematopoietic cells, ACKR3, activated by CXCL11 in malignant cells, enhances cell adhesion, migration, and acts as an HIV coreceptor. ACKR1 Protein, Human (Cell-Free, His) is the recombinant human-derived ACKR1 protein, expressed by E. coli Cell-free, with N-10*His labeled tag. The total length of ACKR1 Protein, Human (Cell-Free, His) is 336 a.a., with molecular weight of 41.1 kDa.

ACKR3 是一种非典型趋化因子受体，通过与趋化因子高亲和力结合，充当趋化因子水平和定位的关键调节因子，导致趋化因子隔离、降解或转胞吞作用。ACKR3 也称为拦截器、趋化因子清除受体或趋化因子诱饵受体，充当 CXCL11 和 CXCL12/SDF1 等趋化因子的受体。与传统配体驱动的信号转导不同，趋化因子与 ACKR3 结合不会激活 G 蛋白介导的通路，而是诱导 β-arrestin 募集，导致配体内化并激活 MAPK 信号通路。ACKR3 在调节迁移中间神经元的 CXCR4 蛋白水平、调整其趋化因子反应性方面发挥着至关重要的作用。在神经胶质瘤细胞中，它通过 MEK/ERK 途径转导信号，有助于细胞生长和存活。虽然不参与正常造血祖细胞功能，但 ACKR3 在恶性造血细胞中被 CXCL11 激活，导致 ERK1/2 磷酸化，增强细胞粘附和迁移。此外，ACKR3 与 CXCR4 一起作为 HIV 分离株的有限子集的共受体，强调了其与微生物感染的参与。

Human

E. coli Cell-free

N-10*His

Q16570 (M1-S336)

2532  [NCBI]

MGNCLHRAELSPSTENSSQLDFEDVWNSSYGVNDSFPDGDYGANLEAAAPCHSCNLLDDSALPFFILTSVLGILASSTVLFMLFRPLFRWQLCPGWPVLAQLAVGSALFSIVVPVLAPGLGSTRSSALCSLGYCVWYGSAFAQALLLGCHASLGHRLGAGQVPGLTLGLTVGIWGVAALLTLPVTLASGASGGLCTLIYSTELKALQATHTVACLAIFVLLPLGLFGAKGLKKALGMGPGPWMNILWAWFIFWWPHGVVLGLDFLVRSKLLLLSTCLAQQALDLLLNLAEALAILHCVATPLLLALFCHQATRTLLPSLPLPEGWSSHLDTLGSKS

41.1 kDa

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

<1 EU/μg, determined by LAL method.