In Stock Cell Lines
Homo sapiens (Human)
Blood (peripheral blood)
Suspension
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.
PAIP1 Knockout K562 Polyclonal Cells
Cat. No. ARG19280
LRPAP1 Knockout SK-HEP-1 Polyclonal Cells
Cat. No. ARG15432
BRD7 Knockout A549 Polyclonal Cells
Cat. No. ARG23117
EHMT2 Knockout HAP1 Polyclonal Cells
Cat. No. ARG40872
CERS5 Knockout HEK293T Polyclonal Cells
Cat. No. ARG4078
PRKAG1 Knockout Hep-G2 Cell Line
Cat. No. ARG0392
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.
