The CCL14 Knockout HAP1 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HAP1 human cell line, engineered for targeted disruption of the CCL14 gene. This loss-of-function model enables investigation of CCL14-dependent mechanisms without altering the host cell??s haploid genetic background. The polyclonal format provides a heterogeneous pool of edited cells, offering a robust system for studying gene function at the population level.
HAP1 is a near-haploid human cell line originating from the KBM-7 chronic myeloid leukemia (CML) derivative, which is BCR-ABL positive and of male origin. Its haploid nature simplifies genetic analysis by requiring mutation of a single allele to achieve functional knockout, making it a powerful platform for genetic screens and pathway dissection. The leukemic background also provides a physiologically relevant context for examining chemokine signaling in hematopoietic malignancies.
CCL14 (HCC-1) is a CC chemokine that recruits monocytes and eosinophils through high-affinity binding to CCR1, CCR3, and CCR5. These G-protein-coupled receptors activate phospholipase C-??, elevating intracellular calcium and stimulating MAPK/ERK and PI3K/Akt signaling cascades. Transcriptional regulation involves TNF-??, IL-1, NF-??B, and STAT3. CCL14 activity is modulated by interaction with glycosaminoglycans and proteolytic processing by urokinase-type plasminogen activator (uPA).
In HAP1 cells, CCL14 knockout eliminates chemokine-driven signaling that may influence leukemic cell functions such as migration and survival. The BCR-ABL-positive background permits investigation of cross-talk between oncogenic and chemokine pathways. Additionally, CCR5 is an HIV coreceptor, making this model relevant for viral entry studies.
These polyclonal knockout cells are suitable for chemotaxis assays, calcium flux measurements, and Western blotting for phospho-ERK to assess signaling. Flow cytometry can track receptor internalization, and RNA-seq comparisons identify transcriptional changes. Cytokine arrays profile altered secretion. This tool supports drug target screening and research in inflammation, cancer immunology, and hematopoiesis. For further details, please contact Ascent Research.
