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Cat. No. ARG1267

DHRS4 Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

The DHRS4 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-mediated polyclonal knockout population of the human Raji B lymphocyte line, featuring disruption of the DHRS4 gene. DHRS4 catalyzes the conversion of retinol to retinal in the retinoic acid synthesis pathway, interacting with CRBP1 and functioning upstream of RDH10 and ALDH1A enzymes to regulate RAR/RXR-mediated transcription. This knockout model enables exploration of retinoid metabolism in B-cell lymphomas, investigation of retinoic acid signaling in immune function, and studies of metabolic reprogramming and drug responses in cancer. Representative assays include retinoic acid quantification, transcriptomic profiling, and cell proliferation measurements.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    Raji

    Cell Type

    B cell line

    Sex of Donor

    Male

    Age

    11 years

    Derived From Site

    In situ; Maxilla

    Gene Name

    DHRS4

    Gene Identifier

    NCBI Gene ID 10901

    Morphology

    Lymphoblast-like

    Growth Mode

    Suspension

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    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 DHRS4 Knockout Raji Polyclonal Cells from Ascent Research are a CRISPR/Cas9-edited polyclonal population of Raji B lymphocytes with targeted disruption of the DHRS4 gene. This heterogeneous knockout pool eliminates the need for single-cell cloning and provides a robust loss-of-function model for studying retinoid metabolism. The polyclonal format preserves genetic diversity and supports large-scale experiments such as functional screens and biochemical assays.

The Raji cell line is an EBV-positive B-lymphoblastoid line derived from a Burkitt lymphoma patient, exhibiting characteristics of mature B cells, including surface immunoglobulin expression and antigen presentation. Widely used in immunology and cancer research, Raji cells serve as a model for B-cell signaling and viral oncogenesis. Their rapid suspension growth facilitates genetic manipulation and downstream analyses, making them an ideal host for DHRS4 knockout to explore retinoid biology in a B-lymphoid context.

DHRS4 encodes an NADH-dependent short-chain dehydrogenase/reductase that catalyzes the oxidation of retinol to retinal, a critical step in all-trans-retinoic acid (atRA) biosynthesis. In the canonical retinoid pathway, DHRS4 interacts with cellular retinol-binding protein 1 (CRBP1) and functions downstream of STRA6-mediated retinol uptake from RBP4. It operates upstream of RDH10 and ALDH1A family enzymes, which produce atRA. Upon synthesis, atRA activates nuclear RAR/RXR transcription factors, regulating genes such as HOX and CYP26. The pathway is further modulated by PPAR?? and feedback from retinoic acid itself. Disruption of DHRS4 therefore impairs retinoic acid production and alters downstream transcriptional programs.

In Raji B lymphocytes, retinoic acid signaling influences proliferation, differentiation, and immune functions, and its dysregulation is associated with lymphoma progression. The DHRS4 knockout model allows researchers to dissect how loss of retinaldehyde production affects B-cell metabolism and tumor biology. Given the lymphoma origin of Raji cells, this system is especially relevant for investigating metabolic reprogramming in cancer and evaluating the role of retinoid metabolism in lymphomagenesis, potentially informing therapeutic strategies targeting these pathways.

This polyclonal knockout product is applicable to studies of retinoid metabolism in B-cell lymphomas, retinoic acid signaling in immune cells, and drug metabolism in cancer. Researchers can validate DHRS4 disruption via Western blotting and RT-qPCR, quantify retinoic acid by LC-MS/MS, measure pathway activity with retinoid reporter assays, assess proliferation using MTS assays, profile transcriptomic changes by RNA-seq, and monitor B-cell markers by flow cytometry. The polyclonal population supports robust, reproducible results. For further information, please contact Ascent Research.

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