mProX™ Human ACKR3 Stable Cell Line

Product Information

Target Protein

ACKR3

Target Family

Chemokine Family

Target Protein Species

Human

Host Cell Type

Huh-7;SNU387;CHO-K1;HEK293

Target Classification

GPCR Cell Lines

Target Research Area

Immunology Research

Related Diseases

Oculomotor-Abducens Synkinesis;Whim Syndrome 1

Gene ID

Human: 57007

UniProt ID

Human: P25106

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

ACKR3, also known as Atypical Chemokine Receptor 3, has been the subject of extensive research due to its diverse roles in various physiological processes. One of the significant findings related to ACKR3 is its role in platelet activation and ischemia-reperfusion tissue injury. Research has shown that ACKR3 acts as a critical regulator of platelet-mediated thrombosis and organ injury following ischemia/reperfusion. Additionally, ACKR3 has been identified to play a role in atherosclerosis. It has been demonstrated that arterial endothelial deficiency of ACKR3 attenuates atherosclerosis due to diminished arterial adhesion and invasion of immune cells. Another area of interest is the potential therapeutic applications of ACKR3. Studies have shown that targeting ACKR3 can lead to the selective elimination of senescent fibroblasts, which has implications in anti-aging and cancer therapies. In conclusion, ACKR3 is emerging as a key molecule in various research areas, from cardiovascular diseases to cancer, making it a potential target for future therapeutic strategies.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

chat Brian (Verified Customer)

What role does ACKR3 play in atherosclerosis? Dec 06 2022

chat Patrick Liam (Creative Biolabs Scientific Support)

ACKR3 is involved in promoting atherosclerosis by mediating the adhesion of immune cells to arterial endothelium, likely through inflammatory MAPK and NF-kB pathways. Dec 06 2022

chat Sharon (Verified Customer)

How does BMP2 influence osteogenic differentiation through ACKR3? May 08 2022

chat Patrick Liam (Creative Biolabs Scientific Support)

BMP2 drives the transduction of mesenchymal stem cells (MSCs) to the osteoblast lineage via the ACKR3/p38/MAPK signaling pathway. May 08 2022

Published Data

Fig.1 The impairment of ACKR3 resulted in a notable impact on the migratory capacity of macrophages.

The Transwell assay evaluated macrophage migration capacity in conditioned media from lentivirus-exposed Huh7 or SNU387 cells. Results are presented as mean ± standard deviation, and statistical significance was determined via unpaired t-test (* p < 0.05).

Ref: Chen, Fu, et al. "Histone deacetylase 2 regulates STAT1-dependent upregulation of atypical chemokine receptor 3 to induce M2 macrophage migration and immune escape in hepatocellular carcinoma." Molecular Immunology 151 (2022): 204-217.

Pubmed: 36179603

DOI: 10.1016/j.molimm.2022.09.005

Research Highlights

Yan J, et al. "Subarachnoid hemorrhage alters CX43 and ACKR3 levels in cerebrospinal fluid: A ." Asian journal of surgery, 2023.
This abstract will be rewritten in the third person as follows: The abstract is limited to a maximum of 80 words and is being rewritten in the third person.
Pubmed: 37777402 DOI: 10.1016/j.asjsur.2023.09.082

Mierzejewski B, et al. "miRNA-126a plays important role in myoblast and endothelial cell interaction.." Scientific reports, 2023.
In this study, the role of miRNA in interactions between muscle satellite cells (SCs) and endothelial cells was investigated. The authors identified miRNAs that were up-regulated in SC-derived myoblasts treated with stromal derived factor-1 (SDF-1) and/or down-regulated in cells where the expression of CXCR4 or CXCR7, both SDF-1 receptors, was silenced. The results showed that miR-126a-3p inhibited myoblast migration and fusion and reduced the levels of Cxcl12 and Ackr3. Interestingly, treatment of endothelial cells with medium conditioned by miR-126a-5p mimic transfected SC-derived myoblasts promoted tubulogenesis. These findings suggest that selected miRNAs play a role in SC-derived myoblast fate and interactions with endothelial cells, and could be potential regulators of skeletal muscle regeneration and angiogenesis.
Pubmed: 37699959 DOI: 10.1038/s41598-023-41626-z