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Cat. No. ARG37854

KDM2B Knockout HEK293T Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Kidney

This CRISPR/Cas9-edited polyclonal KDM2B knockout cell population is derived from HEK293T cells. KDM2B demethylases H3K36me2 and is a core ncPRC1 component, interacting with RING1B and BMI1. Its loss disrupts regulation of CDKN2A, CCND1, and cell proliferation, linking to colorectal and breast cancer. The polyclonal model supports unbiased studies of epigenetic mechanisms, Wnt/??-catenin and TGF-?? signaling, and tumor suppression. Key applications include ChIP-qPCR, co-immunoprecipitation, cell cycle and apoptosis assays, and functional genomics in cancer and neurodevelopmental disorders.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HEK293T

    Sex of Donor

    Female

    Age

    Fetus

    Derived From Site

    Fetal kidney

    Gene Name

    KDM2B

    Gene Identifier

    NCBI Gene ID 84678

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    DMEM

    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 KDM2B Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HEK293T human embryonic kidney cell line, engineered for targeted disruption of the KDM2B gene. This polyclonal pool allows loss-of-function studies without clonal selection bias, enabling investigation of KDM2B??s roles in epigenetic regulation, signaling, and oncogenesis within a broadly used, transfection-competent background. The product supports reproducible functional assays by averaging heterogeneous edit outcomes representative of population-level effects.

HEK293T cells originate from HEK293 cells stably transformed with adenovirus 5 DNA and expressing the SV40 large T antigen, which enables episomal replication of plasmids carrying the SV40 origin. This feature, combined with their embryonic kidney epithelial phenotype, yields exceptionally high transfection efficiency and robust protein production, making them a standard platform for recombinant expression, lentiviral packaging, and functional genomics. The line’s genetic tractability and rapid growth further benefit high-throughput screening applications.

KDM2B encodes a histone lysine demethylase that selectively removes dimethylation from H3K36 (H3K36me2), modulating chromatin structure and transcription. Crucially, it serves as a core component of the non-canonical polycomb repressive complex 1 (ncPRC1), interacting with RING1B, BMI1, PCGF1, RYBP, and CBX7 to recognize unmethylated CpG islands and catalyze H2AK119 monoubiquitination, driving gene silencing. Its activity is regulated by MYC, E2F1, p53, TGF-?? signaling, miR-101, and the miR-30 family. Downstream targets include CDKN2A, CDKN1A, CCND1, CDH1, and HOXA gene clusters. Through these interactions, KDM2B exerts control over cell cycle progression, apoptosis, and stem cell maintenance, and its dysregulation is implicated in colorectal, breast, and other cancers.

In the HEK293T background, KDM2B knockout enables mechanistic dissection of its dual catalytic and scaffolding functions. The cell line??s high transfectability allows efficient re-expression of KDM2B variants for structure-function studies, while the polyclonal nature captures heterogeneous epigenetic responses that better reflect native tissue environments. This model is particularly valuable for investigating crosstalk between the PRC1 system, Wnt/??-catenin pathway components including ??-catenin, and TGF-??/SMAD2/3 signaling, all of which converge on cell fate decisions and oncogenic processes.

Research applications include chromatin immunoprecipitation?CqPCR (ChIP-qPCR) to map H3K36me2 and H3K27me3 changes, combined with RNA-seq and RT-qPCR for transcriptome profiling. Functional assays such as flow cytometry for cell cycle distribution, apoptosis detection, and colony formation quantify KDM2B??s impact on proliferation and survival. Co-immunoprecipitation validates interactions with ncPRC1 members like RING1B and BMI1. The knockout also supports drug target validation and functional genomics screens in colorectal cancer, acute myeloid leukemia, glioblastoma, and neurodevelopmental disorders. For further information, contact Ascent Research.

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