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Cat. No. ARG32969

AP1AR Knockout HT29 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

The AP1AR Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of the HT29 colorectal adenocarcinoma cell line, with disruption of the AP1AR gene. AP1AR encodes an adaptor-related protein that interacts with c-FOS and c-JUN to modulate AP-1 transcription factor activity, controlling cell proliferation, differentiation, and apoptosis. In the HT29 background harboring APC, TP53, and BRAF V600E mutations, this model facilitates studies of AP-1 signaling, colorectal cancer biology, and drug responses. Key applications include Western blotting, co-immunoprecipitation, RNA-seq, cell viability (MTT, CellTiter-Glo), apoptosis (Annexin V), and Transwell migration/invasion assays.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HT29

    Gene Name

    AP1AR

    Gene Identifier

    NCBI Gene ID 55435

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    McCoy's 5A

    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

AP1AR Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population of the human colorectal adenocarcinoma cell line HT29, with targeted disruption of the AP1AR gene. This polyclonal pool provides a genetically heterogeneous loss-of-function model, bypassing single-cell cloning and enabling population-level functional studies of AP1AR in cancer-relevant signaling.

The HT29 cell line was derived from a primary colorectal adenocarcinoma and is widely employed as a model for intestinal epithelial biology and colorectal cancer. HT29 cells grow as adherent epithelia and can be induced to differentiate into enterocyte-like cells. They harbor oncogenic mutations in APC, TP53, and BRAF (V600E), conferring constitutive MAPK pathway activation and providing a clinically relevant background for studying tumorigenesis and signaling dependencies.

AP1AR (Adaptor-related protein complex 1 associated regulatory protein) modulates AP-1 transcription factor activity through direct interaction with c-FOS and c-JUN. It functions downstream of MAPK/ERK and JNK signaling and influences transcription of AP-1 target genes, including MMPs, cyclins, and cytokines. Through this mechanism, AP1AR regulates cell proliferation, differentiation, and apoptosis, processes frequently subverted in cancer. The interacting partner profilin (PFN1) suggests additional links to cytoskeletal reorganization.

In HT29 cells, AP1AR knockout allows dissection of AP-1-dependent transcriptional networks in the context of oncogenic APC, TP53, and BRAF mutations. Loss of AP1AR is anticipated to alter expression of proliferation- and apoptosis-regulating genes, offering insights into AP-1-driven mechanisms of colorectal cancer progression and metastasis. The polyclonal nature of the knockout pool may better mimic tumor heterogeneity, facilitating identification of population-level vulnerabilities and drug sensitivity patterns.

This knockout model supports a broad suite of applications: Western blotting and co-immunoprecipitation for AP-1 complex analysis, RT-qPCR and RNA-seq for transcriptomic profiling, MTT, CellTiter-Glo, and Annexin V staining for viability and apoptosis, and Transwell assays for migration and invasion. Drug sensitivity testing with chemotherapeutics and epithelial barrier function studies are also readily performed. For orders and technical inquiries, please contact Ascent Research.

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