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Cat. No. ARG34197

GRB7 Knockout jurkat Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Blood (peripheral blood)

  • Disease:

    Acute lymphoblastic leukemia (ALL)

GRB7 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited human T lymphocyte population with disrupted GRB7 expression, providing a loss-of-function model for signaling and oncogenesis studies. Derived from the Jurkat leukemia line, these polyclonal knockout cells retain T cell receptor signaling competence while lacking GRB7-mediated adaptor functions. GRB7 links activated RTKs (EGFR, HER2, PDGFR) and FAK to PI3K/AKT and MAPK/ERK pathways via interactions with Shc, Grb2, and p130Cas, regulating migration, proliferation, and survival. These cells are suited for investigating TCR signaling, integrin-mediated migration, and metastasis, supporting assays such as Western blotting, RT-qPCR, and phospho-signaling analysis.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    Jurkat

    Cell Type

    T cell line

    Sex of Donor

    Male

    Age

    14 years

    Derived From Site

    In situ; Peripheral blood

    Gene Name

    GRB7

    Gene Identifier

    NCBI Gene ID 2886

    Growth Mode

    Suspension

    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 GRB7 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population disrupted for GRB7 loss-of-function. Without single-cell cloning, the heterogeneous pool preserves population-level variation while abrogating GRB7 expression. This polyclonal knockout strategy avoids clonal biases, ensuring that functional studies reflect collective cellular responses rather than isolated clonal effects. The model enables robust investigation of GRB7-dependent signaling and phenotypic consequences.

The Jurkat cell line is an immortalized human T lymphocyte line originating from T cell acute lymphoblastic leukemia, widely used for studying TCR signaling and leukemia. With PTEN and INPP5D mutations causing constitutive PI3K/AKT activity, it serves as a model for RTK and adaptor protein signaling. Genetic manipulation and suspension culture are straightforward, facilitating knockout generation for pathway analysis.

GRB7 adaptor protein transduces signals from activated RTKs (EGFR, HER2, PDGFR) and FAK. It binds phosphotyrosines via its SH2 domain, recruiting Shc, Grb2, SOS, and p130Cas to activate PI3K/AKT and MAPK/ERK pathways, thereby regulating migration, proliferation, and survival. GRB7 overexpression is implicated in breast, gastric, and esophageal squamous cell carcinomas, enhancing metastatic potential. Key signaling axes include GRB7??FAK??PI3K/AKT and GRB7??Shc??Grb2??SOS??Ras??ERK.

In Jurkat T cells, GRB7 is engaged in TCR signaling and integrin-mediated adhesion and migration, processes essential for lymphocyte trafficking and leukemic dissemination. Ablation of GRB7 permits thorough analysis of its effects on TCR-induced phosphorylation of AKT and ERK1/2, FAK activation, and cytoskeletal rearrangement. This model elucidates the contribution of adaptor proteins to hematopoietic malignancy signaling and cross-talk between integrin and growth factor pathways, providing a physiologically relevant system for mechanistic investigations.

These polyclonal knockout cells are designed for dissecting GRB7 roles in TCR signaling, integrin-mediated migration in leukemia, and metastasis. Standard assays include Western blotting, RT-qPCR, Transwell migration, invasion, adhesion, and proliferation. Phospho-signaling analysis of pAKT and pERK can be performed via flow cytometry or Western blotting. The cells are a valuable resource for drug discovery targeting GRB7 pathways and for validating pharmacological inhibitors. For further information, please contact Ascent Research.

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