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Cat. No. ARG32839

ACP1 Knockout HT29 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

The ACP1 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from HT29 human colorectal adenocarcinoma cells, targeting the ACP1 protein tyrosine phosphatase. ACP1 dephosphorylates molecules such as EphA2 and FAK, regulating EGFR and insulin receptor signaling, and its loss promotes hyperphosphorylation of downstream targets. This model is ideal for studying tyrosine phosphorylation-dependent pathways in colon cancer, drug screening, and immune evasion. The polyclonal knockout cells enable assays including western blotting, RT-qPCR, proliferation and migration analyses, providing a robust platform for ACP1 functional studies. They are valuable for investigating colorectal cancer mechanisms and phosphatase-related immune modulation. For more details, contact Ascent Research.

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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

    ACP1

    Gene Identifier

    NCBI Gene ID 52

    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 ACP1 Knockout HT29 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line, designed to disrupt the ACP1 gene encoding a low-molecular-weight protein tyrosine phosphatase. This loss-of-function model provides a robust tool for dissecting tyrosine phosphorylation-mediated signaling networks without relying on clonal selection.

HT29 is a broadly utilized epithelial cell line established from a primary colorectal adenocarcinoma. It exhibits intestinal epithelial characteristics and is extensively employed in studies of colon cancer biology, drug absorption, and barrier function. The cell line??s well-defined growth properties and genetic background make it an ideal host for investigating oncogenic signaling perturbations.

ACP1 functions as a protein tyrosine phosphatase that dephosphorylates key signaling intermediates, including the EphA2 receptor, focal adhesion kinase (FAK), STAT5, and the platelet-derived growth factor receptor (PDGFR). Its activity is regulated by upstream stimuli such as epidermal growth factor (EGF), insulin, and cytokines, positioning ACP1 as a negative regulator of major signaling cascades. Through dephosphorylation of these targets, ACP1 modulates downstream pathways including PI3K/AKT, MAPK, and JAK/STAT, thereby influencing cell proliferation, differentiation, and immune responses.

In the context of HT29 colorectal cancer cells, ACP1 knockout is anticipated to result in hyperphosphorylation of its substrates, leading to sustained activation of oncogenic signaling axes. For instance, elevated phosphorylation of EphA2 and FAK may enhance cell migration and invasion, while altered STAT5 phosphorylation could impact survival and immune modulation. The polyclonal knockout population captures the heterogeneity of loss-of-function effects, avoiding biases introduced by single-cell cloning and providing a more physiologically relevant model for studying colorectal cancer progression and immune evasion.

These polyclonal knockout cells are suited for a wide range of experimental applications, including western blotting to assess phospho-tyrosine levels, RT-qPCR for downstream gene expression analysis, proliferation assays such as MTT and BrdU, flow cytometry for cell cycle profiling, and immunoprecipitation of phosphorylated targets. Additionally, migration and invasion assays can be employed to evaluate metastatic potential. Researchers can leverage this model to investigate colon cancer proliferation mechanisms, drug response screening, and the role of tyrosine phosphatases in immune escape. For further information, please contact Ascent Research.

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