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Cat. No. ARG35210

JAK1 Knockout 786-O Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Kidney

  • Disease:

    Renal cell carcinoma

The JAK1 Knockout 786-O Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the JAK1 gene in the 786-O human renal cell carcinoma line. JAK1 encodes a non-receptor tyrosine kinase that mediates cytokine signaling through the JAK-STAT pathway, interacting with receptors like IL-6R and IFNGR1 and phosphorylating STAT1, STAT3, and STAT5. This model enables investigation of JAK1-dependent oncogenic and immune signaling, with applications in target validation and cancer biology. Typical assays include phospho-JAK1 immunoblotting, RT-qPCR for STAT target genes, and flow cytometric analysis of STAT phosphorylation, facilitating dissection of cytokine and growth factor responses.

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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

    JAK1

    Gene Identifier

    NCBI Gene ID 3716

    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 JAK1 Knockout 786-O Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population that introduces a targeted disruption of the JAK1 gene in the 786-O human renal cell carcinoma line. This loss-of-function model provides a heterogeneous cell pool, avoiding clonal selection biases, and enables robust investigation of JAK1-dependent signaling networks. It is an ideal tool for functional genomics, cancer biology, and cytokine signaling studies.

The 786-O cell line is derived from a human clear cell renal adenocarcinoma and displays an adherent epithelial morphology. As a well-characterized kidney cancer model, 786-O retains key oncogenic pathways, including constitutive and cytokine-inducible JAK-STAT signaling. Its reproducible growth characteristics and defined genetic background make it a reliable platform for dissecting signal transduction mechanisms relevant to renal cell carcinoma.

JAK1 encodes a non-receptor tyrosine kinase that associates with cytokine receptor chains such as IL-6R and IFNGR1. Upon ligand binding by IL-6 or IFN-gamma, JAK1 is activated and phosphorylates STAT1, STAT3, and STAT5. These STATs dimerize, enter the nucleus, and regulate genes controlling proliferation and immune responses. Negative regulators include SOCS1 and PIAS, and JAK1 often partners with JAK2. Thus, JAK1 functions as a central signaling hub connecting extracellular cytokine cues to transcriptional programs.

In 786-O renal cell carcinoma, JAK1 signaling promotes tumor growth and immune evasion. Disrupting JAK1 removes a key mediator of cytokine-driven oncogenic pathways, allowing dissection of its role in cancer biology. This model is valuable for studying responses to inflammatory cytokines and assessing JAK1 dependency in processes like proliferation and apoptosis. It also illuminates autocrine/paracrine JAK-STAT activation mechanisms in clear cell renal carcinoma.

Applications include cytokine signal transduction analysis, oncogenic signaling studies, and therapeutic target validation. Assays such as phospho-JAK1 western blotting, RT-qPCR of STAT targets, and flow cytometry for STAT phosphorylation are routinely used. Functional assays like proliferation and apoptosis measurements complement these analyses. For additional details, please contact Ascent Research.

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