VNN1 Knockout THP-1 Cell Line

Product Type:
In Stock Cell Lines
Species:
Homo sapiens (Human)
Tissue Source:
Blood (peripheral blood)
Disease:
Acute monoblastic leukemia
Host Cell:
THP-1
Gene Name:
VNN1
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CRISPR/Cas9-mediated knockout of VNN1 in the human THP-1 monocytic cell line eliminates pantetheinase activity, blocking the conversion of pantetheine to cysteamine and pantothenic acid. Loss of cysteamine disrupts glutathione homeostasis and sensitizes cells to oxidative stress, while altering NF-??B-mediated inflammatory signaling downstream of PPAR??, PPAR??, and TNF-?? regulation. This model is ideal for studying redox biology, inflammation, and coenzyme A metabolism in monocyte and macrophage contexts, with applications in inflammatory bowel disease, colorectal cancer, metabolic syndrome, and atherosclerosis research.

Shipping Info: Cryopreserved in vials and shipped on dry ice

Disclaimer: For Research Use Only
Host CellTHP-1
Sex of DonorMale
Age1 year
Derived From SiteIn situ; Peripheral blood
Gene NameVNN1
Gene IdentifierNCBI Gene ID 8876
Growth ModeSuspension
StorageLiquid nitrogen (LN2)
Temperature37°C
Atmosphere5% CO₂
Sterility testingThe bacterial, yeast, and fungi are not detected in these cells by daily monitor.
Mycoplasma testingNegative for mycoplasma through PCR analysis

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.

By accepting this product, the customer acknowledges and agrees to assume all risks associated with its receipt, handling, storage, disposal, and use.

This product is provided "AS IS". For Research Use Only. Not for human or animal therapeutic use.

Description

The VNN1 Knockout THP-1 Cell Line is a CRISPR/Cas9-edited knockout cell line in which the VNN1 gene has been disrupted to create a stable loss-of-function model. This ready-to-use cell line is derived from THP-1 and provides a genetically defined system for studying pantetheinase-dependent processes. Loss of VNN1 protein expression and enzymatic activity enables investigation of oxidative stress, inflammation, and metabolic pathway alterations.

THP-1 is a human acute monocytic leukemia cell line widely employed as a model for monocyte and macrophage biology. With appropriate stimulation, THP-1 cells differentiate into adherent, macrophage-like cells that exhibit phagocytic activity, cytokine secretion, and ROS production. This inducible differentiation, combined with a well-characterized signaling background, establishes THP-1 as a robust platform for dissecting innate immune functions and redox-sensitive pathways.

VNN1 encodes a GPI-anchored pantetheinase that hydrolyzes pantetheine into pantothenic acid and cysteamine. Cysteamine contributes to glutathione homeostasis and acts as an antioxidant. VNN1 expression is regulated by PPAR??, PPAR??, and TNF-??, and its activity feeds into NF-??B signaling via redox-sensitive intermediates. By abrogating cysteamine production, VNN1 knockout disrupts glutathione regulation and potentiates oxidative stress, thereby modulating NF-??B-driven inflammatory responses.

In THP-1 cells, VNN1 knockout disrupts the pantetheinase?Ccysteamine?Cglutathione axis, impairing redox balance and altering inflammatory signaling. This phenotype is particularly relevant for modeling diseases linked to oxidative stress and chronic inflammation, such as inflammatory bowel disease, colorectal cancer, metabolic syndrome, and atherosclerosis. The dual availability of undifferentiated and differentiated states further enables examination of VNN1 function in both monocytic and macrophage contexts.

The cell line supports a broad range of assays, including Western blot and RT-qPCR for VNN1 validation, pantetheinase activity measurement, glutathione quantification, ROS detection, NF-??B luciferase reporters, cytokine ELISA, and flow cytometry for oxidative stress markers. These tools facilitate research into oxidative stress, macrophage function, coenzyme A metabolism, and cancer biology. For further details on handling, validation, or support, please contact Ascent Research.