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Cat. No. ARG38674

ALB Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

The ALB Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of A-549 lung adenocarcinoma cells with disrupted ALB. Lacking endogenous albumin, this model provides a clean background for studying albumin-mediated transport, pharmacokinetics, and ligand interactions. Albumin, regulated by HNF1 and C/EBP??, transports fatty acids, bilirubin, and drugs, and maintains oncotic pressure and vascular integrity. These cells are ideal as negative controls in immunoassays and for overexpression studies, drug binding assays, and examining non-hepatic albumin functions.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    A549

    Sex of Donor

    Male

    Age

    58 years

    Derived From Site

    Lung

    Gene Name

    ALB

    Gene Identifier

    NCBI Gene ID 213

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM

    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 A-549 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population of A-549 cells carrying a targeted disruption of the ALB gene. This loss-of-function model is generated in the Homo sapiens A-549 lung adenocarcinoma cell line, providing a versatile tool for investigating albumin biology in a non-hepatic epithelial context. The polyclonal format ensures a heterogeneous mixture of edited alleles, offering robust average knockout effects suitable for pooled functional screens and population-level studies.

The A-549 cell line, established from a 58-year-old Caucasian male with lung adenocarcinoma, displays an adherent epithelial morphology and is widely employed as a model of alveolar type II epithelium. These cells are extensively utilized in cancer biology, drug metabolism, and respiratory infection research, making them a well-characterized platform for dissecting molecular mechanisms in pulmonary and systemic disease contexts.

ALB encodes serum albumin, the predominant plasma protein responsible for maintaining colloidal osmotic pressure and serving as a primary carrier for hydrophobic ligands, including fatty acids, bilirubin, hormones, and various pharmaceuticals. Albumin functions downstream of transcriptional regulators such as HNF1, HNF4, C/EBP??, FOXA2, and the glucocorticoid receptor. It interacts with numerous molecular partners, including fatty acids, calcium ions, SPARC, megalin, cubilin, and the FcRn receptor, to modulate ligand bioavailability, antioxidant defense, and vascular permeability.

Since A-549 cells do not endogenously express albumin, this knockout model creates a null background for studying exogenously introduced albumin variants or assessing off-target interactions of albumin-binding compounds. The loss of ALB in this non-physiological context allows dissection of albumin??s role in drug pharmacokinetics, oncotic pressure-independent signaling, and tumor microenvironment modulation without confounding endogenous protein. It is particularly valuable for control experiments in immunoassays and for evaluating albumin-mediated transport in lung epithelial biology.

Typical applications include use as a negative control in western blotting, ELISA, and immunocytochemistry to validate albumin detection reagents. The cells are ideal for overexpressing wild-type or mutant albumin constructs to study trafficking, secretion, and ligand-binding properties. Additionally, they are suited for drug uptake and efflux studies, pharmacokinetic profiling of albumin-binding therapeutics, and investigation of albumin??s antioxidant functions in epithelial injury models. For further inquiries regarding this product, please contact Ascent Research.

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