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Cat. No. ARG43458

CD2AP Knockout 786-O Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Kidney

  • Disease:

    Renal cell carcinoma

CD2AP Knockout 786-O Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population in a clear cell renal cell carcinoma model. This loss-of-function system targets the CD2AP gene, encoding an adaptor that links membrane receptors to the actin cytoskeleton. CD2AP is phosphorylated by Src family kinases and interacts with nephrin, podocin, and cortactin to regulate actin polymerization and endocytosis. Researchers can use these cells to study actin remodeling, cell adhesion, and migration in ccRCC, and to interrogate CD2AP-mediated signaling via co-immunoprecipitation, western blotting, and immunofluorescence.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    786-O

    Sex of Donor

    Male

    Age

    58 years

    Derived From Site

    In situ; Kidney

    Gene Name

    CD2AP

    Gene Identifier

    NCBI Gene ID 23607

    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

CD2AP Knockout 786-O Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the CD2AP gene in Homo sapiens. This population model offers a heterogeneous loss-of-function system, eliminating clonal bias while enabling robust investigation of CD2AP-dependent processes. The polyclonal pool is generated by CRISPR/Cas9-mediated gene disruption, providing a versatile tool for studying gene function at the population level.

The host 786-O cell line originates from a primary clear cell renal cell adenocarcinoma and is a well-characterized model for clear cell renal cell carcinoma (ccRCC). These adherent epithelial cells are widely employed to study renal cancer biology, providing a relevant platform for dissecting the molecular mechanisms underlying tumor progression and cytoskeletal dynamics.

CD2AP functions as an adaptor protein linking membrane receptors to the actin cytoskeleton, essential for podocyte slit diaphragm integrity and T-cell receptor (TCR) signaling. Its activity is regulated by TCR activation and nephrin clustering, followed by phosphorylation by Src family kinases. CD2AP interacts with nephrin, podocin, cortactin, c-Cbl, and the PI3K p85 subunit, coordinating downstream events such as actin polymerization, stabilization of cell adhesion complexes, and endocytic vesicle formation. Through these interactions, CD2AP integrates signals from the nephrin?CNEPH1?Cpodocin complex to regulate actin remodeling and endocytosis.

In 786-O ccRCC cells, CD2AP knockout disrupts the receptor?Ccytoskeleton linkage, potentially altering cell adhesion, migration, and invasion. This polyclonal knockout model mitigates single-clone artifacts, offering a physiologically relevant average response. Given CD2AP??s association with mTOR signaling and endocytic trafficking, its loss may impact growth factor signaling and nutrient sensing, pathways frequently dysregulated in renal carcinoma.

Applications include western blotting and RT-qPCR for knockout validation, immunofluorescence for actin cytoskeleton analysis, and functional assays such as migration and adhesion tests. Co-immunoprecipitation can be used to assess interactions among CD2AP, nephrin, podocin, cortactin, and c-Cbl. The polyclonal nature supports population-level studies of CD2AP??s role in actin dynamics, cell adhesion, and endocytosis in ccRCC. For further details, please contact Ascent Research.

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