The DLG1 Knockout K-562 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population specifically targeting the DLG1 gene in the K-562 host cell background. This loss-of-function model enables detailed investigation of DLG1-dependent molecular mechanisms in a human hematopoietic context. The polyclonal nature of the knockout population preserves genetic heterogeneity while ensuring robust disruption of DLG1 expression, making it suitable for population-level functional genomic studies.
The host cell line, K-562, is a well-established human chronic myelogenous leukemia (CML) cell line originally isolated from the pleural effusion of a patient in blast crisis. K-562 cells are BCR-ABL positive and serve as a model for hematopoietic differentiation, retaining the capacity to differentiate along erythroid and megakaryocytic lineages. This cell line is widely used to study the molecular basis of CML, including oncogenic signaling, drug response, and differentiation pathways.
DLG1 encodes a member of the membrane-associated guanylate kinase (MAGUK) scaffolding protein family that organizes multiprotein complexes at cell junctions and synapses. It plays critical roles in cell polarity, receptor clustering, and signal transduction. DLG1 interacts with a diverse set of proteins, including APC, PTEN, ??-catenin, and several synaptic receptors such as NMDA receptor subunits (GluN2A, GluN2B), AMPA receptor subunits (GluA1), and Shaker-type K+ channels. It functions as a node in the Wnt and Hippo signaling pathways, where it contributes to the regulation of ??-catenin/TCF/LEF transcriptional activity and YAP/TAZ co-activator localization. Upstream regulators include SRC family kinases, CaMKII, and N-cadherin, while downstream targets encompass Ras, PI3K/AKT, and NMDA receptor subunits.
In the K-562 leukemic background, DLG1 knockout disrupts its scaffolding function, potentially altering cell polarity, adhesion, and signaling networks that influence hematopoietic differentiation and malignant transformation. Given the BCR-ABL-driven nature of K-562 cells, loss of DLG1 may intersect with oncogenic signaling pathways, offering a platform to study how polarity and junctional complexes modulate leukemogenesis. This model is particularly relevant for exploring the role of cell architecture in CML and for identifying vulnerabilities that rely on DLG1-mediated protein interactions.
This polyclonal knockout cell product is well-suited for a range of functional assays, including western blotting and co-immunoprecipitation to assess DLG1 protein interactions, RT-qPCR for transcriptional changes in downstream targets such as ??-catenin and PI3K/AKT effectors, immunofluorescence to evaluate junctional protein localization, flow cytometry for differentiation marker expression, and phospho-signaling analysis to map pathway alterations. Applications include investigating cell polarity in leukemia, dissecting DLG1’s role in hematopoietic differentiation, functional analysis of MAGUK proteins in cancer, and drug target validation in CML. For further details or to discuss custom applications, contact Ascent Research.
