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Cat. No. ARG33499

JUND Knockout HT29 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

The JUND Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population created in the HT29 human colorectal adenocarcinoma epithelial cell line. This model enables the study of JUND, a subunit of the AP-1 transcription factor complex, which integrates signals from MAPK/ERK and JNK pathways and regulates downstream targets including CCND1 and IL8. JUND exhibits context-dependent roles as a tumor suppressor or oncogene, making this model valuable for colorectal cancer research. Applications include investigation of AP-1-mediated transcription, proliferation and apoptosis assays, drug target screening, and pathway crosstalk analysis using techniques such as western blotting, RT-qPCR, ChIP-qPCR, and reporter gene 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

    JUND

    Gene Identifier

    NCBI Gene ID 3727

    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% COâ‚‚

  • 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. It 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 JUND Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HT29 human colorectal adenocarcinoma cells, with targeted disruption of the JUND gene. This product provides a loss-of-function model for studying AP-1 transcription factor subunit JUND in a colorectal cancer context. As a polyclonal pool, it retains the genetic heterogeneity of the parental population, enabling robust functional studies without clonal bias.

The HT29 cell line was established from a primary colorectal adenocarcinoma of a 44-year-old Caucasian female and is widely used as a model for intestinal epithelial biology and colorectal cancer. These adherent epithelial cells exhibit intermediate differentiation features, making them suitable for investigating tumor signaling, proliferation, and drug responses in an oncogenic background.

JUND encodes a component of the AP-1 transcription factor complex, which forms dimers with c-JUN, c-FOS, and ATF family members. JUND is activated by upstream kinases ERK1/2, JNK, and p38, which respond to stimuli such as EGF, TGF-alpha, and IL-6. Active JUND-containing complexes regulate transcription of targets involved in cell cycle (CCND1, CDKN1A), apoptosis (BCL2L1), angiogenesis (VEGFA), and inflammation (MMP9, IL8). JUND also interacts with co-regulators p300/CBP, HDAC1, and BACH1, which modulate its activity. The transcription factor participates in crosstalk with Wnt/??-catenin, NF-??B, and STAT3 pathways, contributing to context-dependent tumor-suppressive or oncogenic functions.

In HT29 colorectal adenocarcinoma cells, JUND knockout disrupts a key regulatory node, allowing dissection of AP-1 network contributions to tumor biology. This model is particularly relevant for studying how JUND influences proliferation and survival through effectors like CCND1 and BCL2L1, and for investigating its role in inflammatory signaling via IL-8 and MMP9. The polyclonal nature of the knockout minimizes clonal artifacts, providing a reliable system to analyze JUND??s dual functions in a malignant colorectal epithelium.

Applications include western blotting and RT-qPCR for target protein and gene analysis, ChIP-qPCR for AP-1 binding site occupancy, and functional assays such as MTT-based proliferation, Annexin V apoptosis, and migration/invasion studies. The cells are suited for drug sensitivity profiling, AP-1 luciferase reporter assays, and transcriptomic analysis via RNA-seq. For further information, please contact Ascent Research.

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