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Cat. No. ARG39581

DOCK2 Knockout CaSki Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Squamous cell carcinoma

DOCK2 Knockout Ca Ski Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population in the HPV-16 positive Ca Ski cervical carcinoma line, targeting the DOCK2 gene. DOCK2 acts as a guanine nucleotide exchange factor for Rac1 and Rac2, activated by chemokine receptors (CXCR4, CCR7) and T-cell receptor stimulation, and relays signals through ELMO1, PI3K, and Src family kinases to orchestrate actin cytoskeletal reorganization. This polyclonal knockout model enables the study of lymphocyte migration, chemokine signaling, tumor immune cell infiltration, and DOCK2-related immunodeficiency via Western blotting, RT-qPCR, chemotaxis assays, F-actin staining, and flow cytometry.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    CaSki

    Sex of Donor

    Female

    Age

    40 years

    Derived From Site

    Metastatic; Small intestine

    Gene Name

    DOCK2

    Gene Identifier

    NCBI Gene ID 1794

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    Supplement(s)

    10% Fetal Bovine Serum, 1% Penicillin-Streptomycin Solution

    Temperature

    37°C

    Atmosphere

    5% CO₂

  • Quality Control

    Sterility testing

    The bacterial, yeast, and fungi are not detected in these cells by daily monitor.

    Mycoplasma testing

    Negative for mycoplasma through PCR analysis

  • Disclaimer

    Intended Use

    This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.

    Disclaimer

    Ascent Research endeavors to provide accurate and up-to-date product information. However, no warranties or representations are made regarding its completeness or reliability. References to scientific literature and patents are for informational purposes only, and the customer assumes sole responsibility for verifying their accuracy.

    By accepting this product, the customer acknowledges and agrees to assume all risks associated with its receipt, handling, storage, disposal, and use, including compliance with all applicable safety and environmental regulations and precautions. Relevant laws, regulations, and ethical guidelines must be followed in conducting any research, modifications, or derivatives derived from this product.

    This product is provided "AS IS", and except as expressly stated herein, Ascent Research disclaims all other warranties, express or implied. Under no circumstances shall Ascent Research, its affiliates, or representatives be liable for indirect, incidental, consequential, or punitive damages arising from the use of this material. While Ascent Research employs rigorous quality control measures, we shall not be held responsible for damages resulting from misidentification or misinterpretation of the provided materials.

Description

The DOCK2 Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population created for targeted disruption of the human DOCK2 gene in the Ca Ski cervical carcinoma cell line. This loss-of-function model enables stable, constitutive elimination of DOCK2 protein expression, avoiding the limitations of transient RNA interference. The polyclonal nature ensures a heterogeneous pool of edited cells, reflecting a spectrum of CRISPR-induced disruptions without the bottleneck of clonal selection.

Ca Ski cells are a human cervical epidermoid carcinoma line established from a small intestine metastasis and stably harbor integrated HPV-16 genomes, making them a classic model for HPV-driven cervical carcinogenesis. Their epithelial morphology and tumorigenic capacity support studies of cancer cell proliferation, invasion, and interactions with the microenvironment. The cell line is widely used to investigate molecular mechanisms of oncogenesis and to evaluate therapeutic interventions.

DOCK2 functions as a guanine nucleotide exchange factor (GEF) that activates the small GTPases Rac1 and Rac2. Upon stimulation by chemokine receptors (e.g., CXCR4, CCR7) or the T-cell receptor, DOCK2 is recruited to the plasma membrane via its adaptor protein ELMO1. This localization drives Rac-mediated signaling, engaging downstream effectors such as p21-activated kinase 1 (PAK1), c-Jun N-terminal kinase (JNK), and p38 MAPK, which coordinate actin cytoskeletal remodeling through the ARP2/3 complex. Upstream, DOCK2 activity is regulated by phosphoinositide 3-kinase (PI3K) and Src family kinases, while Vav, CrkL, and talin-1 modulate its function.

In the Ca Ski cervical carcinoma model, DOCK2 knockout provides a platform to study its role in epithelial migration and tumor-immune interactions. Although best characterized in lymphocytes, DOCK2 expression has been reported in some epithelial cancers, and its contribution to chemokine-mediated actin reorganization in an HPV-16-positive background allows investigation of pathways that may impact cervical cancer progression and immune cell recruitment.

This polyclonal knockout product is suited for applications such as Western blotting, RT-qPCR, co-immunoprecipitation, chemotaxis assays, F-actin staining, and flow cytometry. Researchers can employ these cells to study lymphocyte migration and activation, model DOCK2-related immunodeficiency, explore chemokine signaling dynamics, and analyze immune cell infiltration in tumors. For additional information, please contact Ascent Research.

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