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Cat. No. ARG33527

KIAA1522 Knockout HT29 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

The NHSL3 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited population derived from human colorectal adenocarcinoma HT29 cells, featuring targeted disruption of the NHSL3 gene. NHSL3 is a poorly characterized protein predicted to interact with actin and participate in focal adhesion signaling, involving key components such as focal adhesion kinase (FAK) and paxillin. This ready-to-use knockout model is optimized for investigating NHSL3 function in epithelial cell adhesion, migration, and actin cytoskeleton dynamics. It supports diverse applications, including adhesion assays, wound healing, immunofluorescence staining, and drug sensitivity studies in a colorectal cancer context.

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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

    KIAA1522

    Gene Identifier

    NCBI Gene ID 57648

    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 NHSL3 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human colorectal adenocarcinoma cell line HT29, engineered to disrupt the NHSL3 gene. This loss-of-function model enables investigation of NHSL3’s role in actin cytoskeleton organization and cell adhesion. The polyclonal format provides a diverse genetic background, avoiding clonal artifacts while maintaining targeted gene disruption. This product is designed for functional studies in colorectal cancer research.

HT29 cells originate from a primary colorectal adenocarcinoma of a 44-year-old female and exhibit epithelial morphology. Widely used as an intestinal epithelial model, HT29 cells facilitate studies on colorectal cancer biology, intestinal barrier function, and drug responses. Their well-characterized signaling pathways and growth characteristics make them a robust platform for genetic perturbation and phenotypic assays.

NHSL3 belongs to the NHS protein family, which is implicated in actin dynamics and cell adhesion. Although its precise function remains poorly characterized, NHSL3 is predicted to interact with actin and participate in focal adhesion complexes involving proteins such as focal adhesion kinase (FAK) and paxillin. CRISPR-mediated disruption of NHSL3 in HT29 cells may perturb actin filament organization and adhesion signaling, providing a means to examine its contribution to cytoskeletal regulation. Since upstream activators and downstream targets are undefined, this knockout model serves as a critical tool for elucidating NHSL3’s position within the adhesion signaling network.

In the context of HT29 colorectal cancer cells, loss of NHSL3 function may impact epithelial cell behavior, including adhesion, migration, and potentially invasive properties. This model enables researchers to dissect the role of NHSL3 in cancer cell biology, particularly in processes governed by the actin cytoskeleton and focal adhesions. By studying NHSL3-deficient HT29 cells, one can assess alterations in cell morphology, adhesion strength, and wound healing, which are relevant to tumor progression and metastasis.

This polyclonal knockout cell population is suitable for a range of experimental approaches, including cell adhesion assays, scratch wound healing/migration assays, immunofluorescence staining for actin and focal adhesion markers (FAK, paxillin), Western blotting for adhesion proteins, proliferation assays (MTT, colony formation), and drug sensitivity screening. These applications facilitate functional analysis of NHSL3 in colorectal cancer and investigation of actin cytoskeleton regulation. For additional product information and technical support, please contact Ascent Research.

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