The CCM2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat T lymphoblast cell line, engineered to disrupt the CCM2 gene. This product provides a polyclonal pool of cells with targeted gene disruption, enabling loss-of-function studies of CCM2 in a leukemic T cell background. The polyclonal format captures the heterogeneity of editing events across the population, offering a robust model system for investigating CCM2-dependent cellular processes without clonal selection artifacts.
Jurkat cells are an immortalized human CD4+ T lymphocyte line originally established from a patient with T cell leukemia. They serve as a widely used model for studying T cell receptor signaling, apoptosis, and HIV infection due to their rapid growth and well-characterized signaling networks. The lymphoblastoid origin and suspension growth characteristics make Jurkat cells particularly suited for high-throughput assays and biochemical analyses requiring large quantities of cellular material. This host background allows the investigation of CCM2 function within the context of hematopoietic cells, complementing its well-established roles in endothelial biology.
CCM2 encodes a scaffold protein that is a core component of the CCM (cerebral cavernous malformation) complex, interacting with KRIT1 (CCM1) and PDCD10 (CCM3). This complex negatively regulates RhoA-ROCK and MAPK/ERK signaling by recruiting MEKK3. CCM2 also interacts with ICAP1 to modulate integrin ??1 signaling. Loss of CCM2 disrupts this regulation, leading to RhoA hyperactivation, which stimulates ROCK and LIMK, enhancing stress fiber formation and actin-myosin contractility. Concurrently, ERK1/2 and P38 MAPK phosphorylation increase, further promoting cytoskeletal rearrangements and loss of junction integrity. Upstream, CCM2 function is controlled by integrin-mediated adhesion, mechanical stress, and VE-cadherin engagement, positioning it as a key integrator of extracellular cues.
In the Jurkat T lymphoblast model, knockout of CCM2 provides a unique opportunity to dissect its role in non-endothelial systems. Although CCM2 is primarily associated with vascular malformations, its involvement in MAPK and RhoA signaling suggests functions in T cell activation, proliferation, and apoptosis. The Jurkat polyclonal knockout cells enable the study of CCM2-dependent signaling pathways in a leukemic context, which may reveal novel roles in hematological malignancies or immune cell regulation. This model complements endothelial studies by offering a distinct cellular environment where the consequences of CCM2 loss can be assessed in relation to T cell receptor signaling and stress responses.
This CCM2 knockout product is well-suited for a variety of functional assays, including Western blotting to verify CCM2 depletion, RhoA activation assays to assess GTPase activity, and phospho-ERK analysis to monitor MAPK pathway output. Flow cytometry can be used for cell cycle and apoptosis profiling, while adhesion and migration assays evaluate cytoskeletal-dependent processes. The model is applicable to T cell signaling research, leukemic cell biology investigations, and drug screening campaigns targeting CCM pathway components. The polyclonal knockout format provides a heterogeneous genetic background, avoiding clonal selection bias. For further information, please contact Ascent Research.
