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Cat. No. ARG40901

EIF2A Knockout AGS Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Stomach

  • Disease:

    Adenocarcinoma

The EIF2A Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from AGS human gastric adenocarcinoma epithelial cells, featuring targeted disruption of the EIF2A gene. EIF2A encodes eIF2??, the master regulator of the integrated stress response (ISR) that controls translation initiation upon phosphorylation by stress kinases like EIF2AK3 (PERK) and EIF2AK4 (GCN2). This knockout model enables rigorous analysis of ISR-dependent signaling in gastric cancer, including ATF4 and CHOP induction, and facilitates drug screening for eIF2?? phosphorylation modulators. The polyclonal pool supports studies of stress adaptation in a heterogeneous cellular context relevant to tumor biology.

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Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    AGS

    Sex of Donor

    Female

    Age

    54 years

    Derived From Site

    In situ; Stomach

    Gene Name

    EIF2A

    Gene Identifier

    NCBI Gene ID 83939

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    Ham's F-12

    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 EIF2A Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the EIF2A gene is disrupted. This product provides a heterogeneous pool of AGS human gastric adenocarcinoma epithelial cells carrying loss-of-function edits, enabling robust investigation of EIF2A-dependent processes without clonal isolation.

AGS cells are an established model of gastric adenocarcinoma, retaining epithelial characteristics and tumorigenic properties. They are widely employed to study gastric cancer biology, drug responses, and stress adaptation mechanisms relevant to tumor survival in the microenvironment.

EIF2A encodes eIF2??, the regulatory subunit of the eukaryotic initiation factor 2 complex. eIF2?? is a central mediator of the integrated stress response (ISR). Upon diverse stresses, kinases EIF2AK3 (PERK)/ER stress, EIF2AK4 (GCN2)/amino acid deprivation, EIF2AK2 (PKR)/viral dsRNA, and EIF2AK1 (HRI)/heme deficiency phosphorylate eIF2?? at Ser51. This phosphorylation inhibits the guanine nucleotide exchange factor eIF2B, causing global protein synthesis attenuation while enhancing translation of select mRNAs with upstream ORFs, notably ATF4. ATF4 induces DDIT3 (CHOP) and PPP1R15A (GADD34), which feed back to dephosphorylate eIF2??. eIF2?? interacts with eIF2S2 (??), eIF2S3 (??), eIF5, and ribosomes. Thus, EIF2A orchestrates translational reprogramming in response to cellular stress.

Elimination of EIF2A in AGS cells disrupts the ISR, allowing dissection of how eIF2??-mediated translation control affects gastric cancer cell growth, apoptosis, and adaptation to microenvironmental stresses such as nutrient deprivation and chemotherapy. The polyclonal knockout population reflects genetic heterogeneity found in tumors, strengthening the translational relevance of stress response studies.

Applications include investigating ISR signaling in gastric adenocarcinoma, validating translational control targets, and screening modulators of eIF2?? phosphorylation. Representative assays include western blot for phospho-eIF2??, RT-qPCR for ATF4 and CHOP, tunicamycin-induced ER stress tests, polysome profiling, cell viability under stress, and ATF4-luciferase reporters. For further information, contact Ascent Research.

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