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Cat. No. ARG1121

NIPA1 Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

NIPA1 Knockout Raji Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal Raji B lymphocyte population harboring targeted disruption of the NIPA1 gene, which encodes a magnesium transporter and negative regulator of BMP signaling. The Raji host line, derived from Burkitt??s lymphoma and latently infected with Epstein-Barr virus, is a widely used model for B cell malignancies and apoptosis. Loss of NIPA1 impairs BMP receptor (BMPR2) endocytic degradation, leading to enhanced SMAD1/5/8 phosphorylation and ID family gene expression. These polyclonal knockout cells are ideal for western blotting, luciferase reporter assays, flow cytometry, and drug discovery applications focused on BMP pathway modulation, magnesium transport, and lymphoma biology.

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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

    NIPA1

    Gene Identifier

    NCBI Gene ID 123606

    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% 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

NIPA1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Raji B lymphocytes with targeted disruption of the NIPA1 gene. This loss-of-function model enables investigation of magnesium transporter activity and bone morphogenetic protein (BMP) signaling regulation in a human lymphoid background. The polyclonal format provides a heterogeneous pool of edited cells suitable for population-level functional genomics and drug screening.

The Raji cell line, derived from Burkitt??s lymphoma, harbors Epstein-Barr virus (EBV) and exhibits a type III latency pattern. Raji cells grow as suspension lymphoblasts and are widely used to study B cell malignancies, EBV-dependent transformation, and apoptotic signaling. Their rapid proliferation and well-characterized transcriptome facilitate CRISPR/Cas9-mediated gene knockout and subsequent functional assays.

NIPA1 encodes a magnesium transporter that negatively regulates BMP signaling by binding to BMP type II receptors (BMPR2) and promoting their endocytic degradation via the adaptor ZFYVE9/SARA. This reduces BMP2- and BMP4-dependent phosphorylation of SMAD1, SMAD5, and SMAD8, limiting their complex formation with SMAD4 and subsequent transcriptional activation of ID family target genes. NIPA1 activity is modulated by cellular magnesium concentrations and interacts with hereditary spastic paraplegia proteins ATL1 and SPAST. Disruption of NIPA1 in Raji cells relieves pathway inhibition, leading to enhanced SMAD signaling and altered transcriptional programs.

In Raji B lymphocytes, BMP signaling regulates proliferation, differentiation, and apoptosis. Loss of NIPA1 likely elevates SMAD phosphorylation and ID gene expression, potentially influencing cell fate determination and EBV latency maintenance. This model is valuable for dissecting crosstalk between magnesium homeostasis, BMP pathway activity, and B cell lymphoma biology, and provides a non-neuronal system to investigate hereditary spastic paraplegia-related mechanisms.

Researchers may utilize NIPA1 Knockout Raji Polyclonal Cells in western blotting to assess SMAD1/5/8 phosphorylation, RT-qPCR for ID gene expression, luciferase reporter assays to measure SMAD-responsive transcription, co-immunoprecipitation to examine NIPA1?CBMPR2 complexes, and flow cytometry for apoptosis or proliferation endpoints. Key applications include mechanistic studies of BMP signaling in B lymphocytes, functional analysis of magnesium transporter activity, drug screening for BMP pathway modulators, and lymphoma-focused functional genomics. For further technical details, please contact Ascent Research.

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