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Cat. No. ARG43343

CCR9 Knockout HT29 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

The CCR9 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population in HT29 colorectal adenocarcinoma cells, targeting the CCL25 receptor CCR9. This chemokine receptor mediates lymphocyte migration to the intestine and orchestrates mucosal immune responses. Loss of CCR9 disrupts signaling through Gi, Gq, and G12/13 proteins, impairing MAPK/ERK and PI3K/Akt pathway activation and downstream effectors such as NF-??B and AP-1. This knockout model is highly valuable for investigating colorectal cancer mechanisms, inflammatory bowel disease, and chemokine biology, with direct utility in migration/chemotaxis assays, calcium flux analysis, and co-culture experiments.

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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

    CCR9

    Gene Identifier

    NCBI Gene ID 10803

    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

The CCR9 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the CCR9 gene in HT29 colorectal adenocarcinoma cells. This loss-of-function model facilitates investigation of CCR9’s role in chemokine signaling and intestinal epithelial biology. The polyclonal nature provides a heterogeneous gene-disrupted pool suitable for reproducible functional studies without transient knockdown limitations.

The HT29 cell line, derived from a primary colorectal adenocarcinoma of a 44-year-old female, is a well-established intestinal epithelial model. These cells retain differentiated functions such as mucus production and polarization, making them ideal for studying gut-specific pathways. Their colorectal adenocarcinoma origin provides a physiologically relevant context for examining CCR9-mediated processes in intestinal pathophysiology.

CCR9 encodes a G protein-coupled receptor for the chemokine CCL25 (TECK), crucial for lymphocyte homing to the gut. Ligand binding activates Gi, Gq, and G12/13 proteins, triggering PLC-??-mediated calcium mobilization and downstream MAPK/ERK (Ras-Raf-MEK-ERK) and PI3K-Akt cascades. CCR9 also recruits ??-arrestin-2 and GRK2 for signal regulation. These pathways lead to NF-??B and AP-1 transcription factor activation, Rho/Rac GTPase-mediated cytoskeletal changes, and integrin ??4??7 upregulation, thereby controlling directed migration, survival, and gene expression in intestinal immunity.

In HT29 cells, CCR9 signaling may influence tumor cell migration, invasion, and immune microenvironment interactions. Knocking out CCR9 enables dissection of its role in colorectal cancer progression and inflammatory bowel disease-related pathways. This model allows researchers to isolate CCL25/CCR9-driven signaling and crosstalk with other chemokine axes, clarifying how CCR9 integrates into epithelial cell networks controlling intestinal homeostasis and disease.

This knockout population supports diverse research applications, including drug target validation, migration/invasion assays (Boyden chamber), calcium flux analysis, phospho-ERK/Akt detection, and RhoA/Rac activation assays. It is suitable for co-culture with immune cells, RNA-seq profiling, and high-throughput screening. The polyclonal format ensures robust and reproducible results for mechanistic studies and pathway interrogation. For further inquiries, please contact Ascent Research.

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