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Cat. No. ARG37413

BMAL2 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The BMAL2 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting BMAL2 in HeLa human cervical adenocarcinoma cells. BMAL2 is a core circadian transcription factor that heterodimerizes with CLOCK to activate clock genes such as PER1/2 and CRY1/2, forming a negative feedback loop. The HeLa host features HPV18 integration and inactivated p53/Rb, providing a cancer-relevant background. Applications include circadian rhythm research, cancer cell proliferation and drug sensitivity assays, and metabolic studies. Representative assays supported are Western blotting, RNA-seq, luciferase reporters, and flow cytometry. This polyclonal knockout pool minimizes clonal biases, offering a robust model to dissect BMAL2??s role in circadian-linked tumor biology.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HeLa

    Sex of Donor

    Female

    Age

    31 years

    Gene Name

    BMAL2

    Gene Identifier

    NCBI Gene ID 56938

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM (with NEAA)

    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 BMAL2 Knockout HeLa Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population targeting the BMAL2 gene in HeLa cells. BMAL2 (ARNTL2/MOP9) is a core circadian transcription factor. This polyclonal product comprises a heterogeneous pool of cells with disrupted BMAL2 alleles, facilitating loss-of-function studies without clonal selection bias. The knockout is generated via CRISPR/Cas9-mediated gene disruption, resulting in abrogated protein expression.

HeLa is an immortalized human cervical epithelial adenocarcinoma line widely employed in cancer research. These cells contain integrated HPV18 DNA, whose E6 and E7 oncoproteins inactivate the tumor suppressors p53 and Rb, respectively, conferring high proliferative capacity and experimental tractability. The well-characterized genomic background of HeLa cells provides a reproducible platform for investigating gene function and drug responses.

BMAL2 heterodimerizes with CLOCK or NPAS2 to bind E-box elements, recruiting coactivators such as CBP/p300 to activate transcription of clock genes including PER1, PER2, CRY1, CRY2, and DBP. The expressed PER and CRY proteins subsequently inhibit the BMAL2-CLOCK complex, forming a negative feedback loop that drives circadian oscillations. BMAL2 activity is regulated by upstream factors like REV-ERB??, ROR??, CKI??, and GSK3??, and it participates in HIF-1 signaling, metabolic control, and cell cycle regulation.

In HeLa cells, BMAL2 knockout disrupts circadian transcriptional networks in a transformed background with defective p53 and Rb pathways. This model enables investigation of how circadian clock disruption influences cancer cell proliferation, genomic stability, and therapeutic responses. The polyclonal nature of the knockout population reduces the risk of clonal artifact interference, ensuring that phenotypes are representative of the overall gene-disruption effect.

Researchers can use these cells for circadian rhythm analysis via luciferase reporter assays and RNA-seq, and for mapping clock protein-DNA interactions by ChIP-qPCR. Cancer biology applications include proliferation and drug sensitivity testing, cell cycle analysis by flow cytometry, and metabolic profiling. These cells also serve as negative controls for BMAL2 antibody validation in Western blotting. For additional information or customization, please contact Ascent Research.

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