The CCL21 Knockout HAP1 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population in which the CCL21 gene has been disrupted via CRISPR/Cas9-mediated gene editing in the near-haploid HAP1 cell line. This product provides a polyclonal pool of CCL21-null cells, enabling loss-of-function studies of the chemokine CCL21 without the need for single-cell clone isolation. The polyclonal format preserves genetic diversity while achieving effective target-gene disruption, making it suitable for a broad range of functional genomics and cell-based assays.
HAP1 cells are derived from a male patient with chronic myeloid leukemia and exhibit a near-haploid karyotype, which eliminates functional redundancy from a second allele, greatly facilitating unambiguous gene knockout studies. Adapted to adherent growth, HAP1 cells serve as a robust model for genetic perturbation and have been widely employed in functional genomics, drug screening, and signal transduction research. Their haploid nature enhances the efficiency and clarity of CRISPR/Cas9-mediated gene disruption, making them an ideal host for generating polyclonal knockout populations.
CCL21 is a homeostatic chemokine that orchestrates lymphocyte homing to secondary lymphoid organs by binding its cognate receptor CCR7. Upon CCL21 stimulation, CCR7 activates downstream signaling cascades including the ERK1/2 and PI3K/Akt pathways, as well as Rho GTPases such as Rac1, leading to actin cytoskeleton rearrangement and directional cell migration. Upstream, CCL21 expression is induced by pro-inflammatory cytokines including TNF-alpha, lymphotoxin-beta, and IL-1beta. CCL21 interacts not only with CCR7 but also with glycosaminoglycans and integrins, which facilitate its presentation and function on endothelial surfaces. Key pathway components include ERK1/2, PI3K, Akt, and Rac1, which collectively mediate chemotactic responses.
In the HAP1 background, disruption of CCL21 provides a clean loss-of-function model to dissect its role in lymphocyte trafficking and immune cell migration. The haploid genome of HAP1 cells ensures that the knockout effect is unambiguous, avoiding confounding expression from a second allele. This model enables researchers to directly link CCL21 deficiency to alterations in downstream signaling events and cellular behavior without the complexity of diploid compensation. The polyclonal nature further allows assessment of population-level responses, which can be more physiologically relevant than monoclonal derivations.
Researchers can employ this CCL21 knockout cell pool in a variety of experimental contexts, including transwell migration assays to measure chemotactic deficiencies, flow cytometry and immunofluorescence to assess receptor expression and cytoskeletal changes, and phospho-signaling analysis to evaluate ERK1/2 and Akt activation. In drug discovery, these cells are valuable for screening CCR7 antagonists or exploring compounds that modulate lymphocyte migration. They also serve as a model for studying cancer metastasis, where CCL21-CCR7 signaling promotes lymph node dissemination. For additional information or technical assistance, please contact Ascent Research.
