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Cat. No. ARG35283

ALB Knockout AGS Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Stomach

  • Disease:

    Adenocarcinoma

The ALB Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from AGS human gastric adenocarcinoma cells, targeting the albumin (ALB) gene. Albumin is a critical plasma protein for oncotic pressure and transport of fatty acids, hormones, and drugs, regulated by factors like HNF1 and IL-6, and interacts with receptors including FcRn and gp60. These polyclonal knockout cells provide a robust model for studying albumin-mediated transcytosis, drug delivery, and tumor microenvironment interactions. Researchers can leverage this tool for assays such as fatty acid uptake, H. pylori infection studies, and serum-free culture optimization, with validation by western blot, ELISA, and immunofluorescence.

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Shipping Info:

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

    ALB

    Gene Identifier

    NCBI Gene ID 213

    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 ALB Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population generated from the AGS human gastric adenocarcinoma cell line, in which the ALB gene encoding albumin has been disrupted. This polyclonal product provides a mixed population of knockout cells, avoiding clonal artifacts and offering a robust loss-of-function model for investigating albumin-related biology.

AGS cells are a widely used epithelial model of gastric adenocarcinoma, originally derived from a patient stomach. They are instrumental in studying gastric carcinogenesis, H. pylori infection dynamics, and host-pathogen interactions, and their well-characterized growth properties make them an ideal host for genetic perturbation.

Albumin is the predominant plasma protein, essential for maintaining colloidal osmotic pressure and serving as a carrier for hydrophobic molecules including fatty acids, hormones, and drugs. Its expression is regulated by transcription factors HNF1, HNF3, C/EBP, and modulated by insulin, glucocorticoids, and inflammatory cytokines such as IL-6 and TNF-alpha. Albumin interacts with several key binding partners: FcRn controls its recycling and systemic persistence; gp60 (albondin) mediates endothelial transcytosis; and SPARC modulates extracellular matrix interactions. These molecular associations drive pathways like FcRn-mediated recycling, gp60-dependent endocytosis, and the formation of albumin-fatty acid complexes, ultimately governing ligand biodistribution and cellular uptake.

In the AGS background, which lacks endogenous albumin expression, this knockout model eradicates any residual ALB activity, creating a clean genetic null for functional studies. It enables researchers to examine how exogenous albumin influences gastric cancer cell behavior, such as transcytosis through the epithelial barrier, drug delivery mediated by gp60, and tumor microenvironment crosstalk via SPARC. Additionally, the knockout facilitates serum-free culture optimization by eliminating confounding variables from albumin in serum, permitting refined analysis of nutrient and signaling requirements.

Typical applications include quantitative albumin uptake and transcytosis assays employing fluorescent or radiolabeled ligands, fatty acid uptake measurements, and drug binding experiments for nanoparticle or conjugate delivery systems. The model is valuable for H. pylori infection studies, where albumin status may affect bacterial adhesion or host responses, and for modeling the tumor microenvironment, particularly interactions involving SPARC and gp60. Transcriptomic profiling via RNA-seq can reveal ALB-dependent pathways, while standard validation uses western blotting, albumin ELISA, and immunofluorescence. For further details or technical assistance, please contact Ascent Research.

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