The CCL1 Knockout HAP1 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the human CCL1 gene in the HAP1 cell line. This gene-edited pool offers a versatile loss-of-function model for investigating CCL1-dependent signaling and functional responses without relying on isolated clones, enabling robust and reproducible studies in a near-haploid background.
HAP1 is a human near-haploid chronic myeloid leukemia (CML) cell line derived from the KBM-7 line, widely used for genetic knockout studies due to its haploid genome simplifying gene disruption. Its CML origin makes it relevant for leukemia research, while its adherent growth and intact signaling pathways facilitate diverse assay formats. The line retains key features of leukemic cells, providing a physiologically meaningful context for chemokine research.
CCL1 encodes a chemokine that chemoattracts monocytes, macrophages, and Th2 cells by binding the CCR8 receptor. This interaction activates G??i-mediated signaling, triggering PLC??, IP3-mediated intracellular calcium release, and downstream activation of PI3K/AKT and MAPK/ERK cascades. Transcription factor NF-??B is also engaged, promoting cell migration and survival. Upstream regulators include IL-4 and STAT6, while downstream targets encompass ERK1/2, AKT, and calcium mobilization. Interacting factors such as ??-arrestin and G protein-coupled receptor kinases modulate signaling dynamics.
In the HAP1 background, CCL1 knockout disrupts endogenous chemokine signaling, providing a clean system to dissect CCR8-mediated pathways. Since HAP1 cells express key signaling intermediates, this knockout model enables precise interrogation of the CCL1/CCR8 axis in leukemic cell behavior, including migration and survival. It can be used to study how chemokine signaling influences leukemia progression and immune cell trafficking, offering insights into the tumor microenvironment and inflammatory processes.
Typical applications include chemotaxis and migration assays to assess CCL1-dependent cell movement, calcium flux measurements to monitor early signaling events, and western blot analysis of phospho-ERK and phospho-AKT to evaluate downstream pathway activation. This model is suited for validating drug targets in allergic inflammation, atopic dermatitis, asthma, and cancer, particularly in tumor microenvironment and immune cell recruitment studies. Knockout validation can be performed by RT-qPCR and sequencing. For additional details or custom inquiries, please contact Ascent Research.
