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Cat. No. ARG1262

PAFAH2 Knockout Raji Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone

  • Disease:

    Burkitt lymphoma

The PAFAH2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited pool of EBV-positive Raji B lymphocytes with disrupted PAFAH2, the gene encoding platelet-activating factor acetylhydrolase 2. Loss of PAFAH2 elevates PAF, sustaining PAF receptor signaling through G??q/11 and G??i proteins to activate calcium flux, MAPK (ERK, p38) phosphorylation, and NF-??B-driven cytokine expression (e.g., IL-6, IL-8). This polyclonal model is suited for functional analysis of PAF signaling in B-cell lymphoma, inhibitor screening, and drug target validation. Assays include PAF quantification, calcium flux, NF-??B reporter, and phospho-MAPK detection, along with proliferation and apoptosis studies. It also permits investigation of EBV?CPAF crosstalk in B-cell transformation.

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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

    PAFAH2

    Gene Identifier

    NCBI Gene ID 5051

    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

The PAFAH2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of Raji B lymphocytes with targeted disruption of the PAFAH2 gene. This loss-of-function model provides a heterogeneous pool of edited cells suitable for pooled functional assays and population-level studies in PAF signaling research.

Raji cells are a suspension B?lymphocyte line derived from a Burkitt lymphoma patient and latently infected with Epstein?Barr virus (EBV). They express B?cell markers and model B?cell malignancies and EBV?associated lymphoproliferative disorders, offering a clinically relevant system for oncogenic and inflammatory pathway analysis.

PAFAH2 encodes a cytosolic acetylhydrolase that hydrolyzes platelet?activating factor (PAF) and oxidized phospholipids, terminating their pro?inflammatory actions. Knockout of PAFAH2 results in elevated PAF levels and sustained activation of the PAF receptor (PAFR), which couples to G??q/11 and G??i proteins. This triggers phospholipase C activation, inositol trisphosphate?mediated calcium mobilization, and protein kinase C?dependent stimulation of MAPK cascades including ERK and p38 phosphorylation. Downstream, NF???B and AP?1 transcription factors drive expression of pro?inflammatory cytokines such as IL?6 and IL?8. The pathway is modulated by upstream regulators like TNF???, IL?1??, and LPS, and intersects with arachidonic acid metabolism through COX?2, producing prostaglandins and leukotrienes that amplify inflammatory signals.

In Raji lymphoma cells, constitutive PAFR signaling due to PAFAH2 loss provides a tool to study lipid mediator contributions to B?cell proliferation, survival, and transformation. The interaction with EBV latency, which also manipulates NF???B and MAPK pathways, can be probed to evaluate potential tumor?suppressive or regulatory roles for PAFAH2 in lymphomagenesis.

Assays applicable to this polyclonal model include PAF quantification by ELISA or LC?MS, intracellular calcium flux measurement, NF???B luciferase reporter assays, and phospho?MAPK Western blotting. Functional studies may employ proliferation (MTS, BrdU), apoptosis (Annexin V/propidium iodide), and cytokine secretion (IL?6/IL?8 ELISA) readouts, along with PAF receptor antagonist sensitivity testing. Applications span functional analysis of PAF signaling in B?cell lymphoma, inhibitor screening, drug target validation for inflammatory and lymphoproliferative diseases, and investigation of EBV?related B?cell transformation. For further information, please contact Ascent Research.

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