The CD33 Knockout HAP1 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population in which the CD33 gene has been disrupted through targeted Cas9 endonuclease activity. As a polyclonal pool, this product contains a variety of independent editing events at the CD33 locus, providing a heterogeneous mixture of knockout alleles. This format is particularly useful for applications that benefit from genetic diversity, such as pooled functional screens or pathway analyses, while still enabling loss-of-function investigation. The cells are supplied as a viable, near-haploid adherent culture derived from the HAP1 cell line, and researchers are advised to confirm CD33 expression status using standard validation methods before interpretation of experimental results.
The HAP1 host cell line is a human chronic myeloid leukemia-derived adherent cell line, originally derived from the near-haploid KBM-7 CML line. Its near-haploid karyotype simplifies functional genomics studies by reducing genetic redundancy and facilitating gene-editing applications. HAP1 cells are widely used in cancer research as a model for hematopoietic malignancies and for genome-wide screening campaigns. The adherent growth properties and stable chromosome number make HAP1 an ideal platform for CRISPR/Cas9-based gene disruption studies, and this CD33 knockout derivative extends the utility of the HAP1 model to myeloid immunoreceptor research.
CD33 encodes a sialic acid-binding immunoglobulin-like lectin (Siglec-3) that functions as an inhibitory receptor on the surface of myeloid cells. Upon binding to sialylated glycans, its immunoreceptor tyrosine-based inhibitory motifs (ITIMs) are phosphorylated, recruiting the tyrosine phosphatases SHP-1 and SHP-2. These phosphatases dephosphorylate key signaling mediators such as Syk kinase, leading to suppression of downstream pathways including PI3K/AKT and attenuation of immune cell activation. The CD33 inhibitory axis also intersects with Vav and ERK signaling components, constituting a core inhibitory module in myeloid cells. Thus, CD33 serves as a critical checkpoint limiting myeloid cell activation, adhesion, and phagocytosis, with well-established roles in immune homeostasis and disease.
In the HAP1 myeloid leukemia background, disruption of CD33 removes a major inhibitory constraint, which can potentiate proximal signaling events and effector functions. This knockout model is valuable for dissecting leukemic signaling mechanisms and for exploring immunotherapeutic strategies aimed at blocking CD33-mediated immune suppression. Given the implication of CD33 in acute myeloid leukemia and Alzheimer’s disease, these polyclonal knockout cells provide a scalable system to study the molecular consequences of CD33 deficiency, supporting target validation and drug discovery.
Typical applications include signal transduction analysis using phospho-specific antibodies to SHP-1, SHP-2, or Syk, as well as assays for sialic acid binding and phagocytosis. The cells are suitable for flow cytometry, western blotting, and RT-qPCR. These approaches enable investigation of CD33 function in myeloid biology, Alzheimer’s disease risk via microglial signaling, and AML immunotherapy. For compound screening or genetic interaction studies, this model provides a flexible platform. For further information, contact Ascent Research.
