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Cat. No. ARG39568

DOCK2 Knockout KYSE150 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Esophagus

  • Disease:

    Squamous cell carcinoma

CRISPR/Cas9-edited polyclonal knockout cell pool for DOCK2 in the human KYSE-150 esophageal squamous cell carcinoma line. DOCK2 is a Rac-specific GEF that drives actin polymerization, lamellipodia formation, and cell migration via ELMO1 and downstream PAK-WAVE-Arp2/3 signaling. This knockout model disrupts Rac-mediated cytoskeletal dynamics, making it ideal for studying mechanisms of metastasis and invasion in esophageal cancer. Typical applications include wound healing, transwell migration/invasion assays, Rac activation pull-down, immunofluorescence staining of F-actin, and biochemical analysis of the DOCK2-ELMO-Rac-PAK signaling axis. For further details, contact Ascent Research.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    KYSE-150

    Sex of Donor

    Female

    Age

    49 years

    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:Ham's F-12(1:1)

    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 KYSE-150 Polyclonal Cells are a pool of CRISPR/Cas9-edited polyclonal knockout cells derived from the human KYSE-150 esophageal squamous cell carcinoma line. This population features targeted disruption of the DOCK2 gene, which encodes a Rac-specific guanine nucleotide exchange factor (GEF). The polyclonal knockout format provides a heterogeneous loss-of-function model suitable for functional studies without clonal selection.

KYSE-150 is a well-established human esophageal squamous cell carcinoma cell line originating from a well-differentiated invasive tumor. It serves as a representative model for esophageal cancer research, enabling investigation of molecular mechanisms underlying tumor progression, metastasis, and therapeutic response.

DOCK2 functions as a critical activator of Rac GTPases, catalyzing GDP/GTP exchange to promote Rac1 and Rac2 activation. Upon stimulation by upstream chemokine receptors (CXCR4, CCR7), T cell receptor, B cell receptor, integrins, or growth factor receptors, DOCK2 forms a complex with ELMO1 and CRK, leading to Rac-mediated signaling. Activated Rac subsequently triggers downstream effectors including PAK1, the WAVE complex, and the Arp2/3 complex, culminating in actin polymerization, lamellipodia formation, and enhanced cell motility. This pathway integrates signals from the PI3K-AKT axis and phosphoinositide lipids such as PIP3, orchestrating cytoskeletal reorganization and directed migration.

In the KYSE-150 esophageal squamous cell carcinoma context, DOCK2-mediated Rac signaling is instrumental for tumor cell migration and invasion, key processes in metastasis. Disruption of DOCK2 expression in this model impairs actin dynamics and lamellipodia formation, thereby attenuating the invasive capacity of the cancer cells. This knockout cell population thus provides a valuable tool for dissecting the contribution of the DOCK2-ELMO1-Rac1 pathway to esophageal cancer aggressiveness and for evaluating therapeutic strategies targeting metastatic dissemination.

Typical research applications include wound healing and transwell migration/invasion assays to measure motile and invasive behavior, Rac activation assays (GST-PBD pull-down) to assess GTP-Rac levels, and immunofluorescence with phalloidin to visualize F-actin structures. Further biochemical analyses such as western blotting for DOCK2, Rac, PAK, and phospho-PAK, co-immunoprecipitation of DOCK2-ELMO complexes, and RT-qPCR or RNA-seq for transcriptional profiling are enabled. These cells also support drug sensitivity and apoptosis studies in esophageal cancer research. For technical inquiries, please contact Ascent Research.

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