In Stock Cell Lines
Homo sapiens (Human)
Pleural effusion
Adherent
The PRDX1 Knockout ACHN Cell Line is a CRISPR/Cas9-edited knockout cell line established from the human renal epithelial adenocarcinoma ACHN cell line, originally derived from a metastatic pleural effusion. This model ablates peroxiredoxin-1, an antioxidant peroxidase that binds and inhibits ASK1, thereby controlling JNK/p38 and NF-??B signaling pathways crucial for apoptosis, proliferation, and redox homeostasis. It enables cancer biology and oxidative stress research, with assays such as ROS quantification, apoptosis detection, and phospho-kinase profiling to dissect signaling. The line provides a relevant model for studying redox-driven cancer mechanisms and potential therapeutic interventions.
ATP1B1 Knockout HEK293T Polyclonal Cells
Cat. No. ARG25792
FKBP4 Knockout jurkat Polyclonal Cells
Cat. No. ARG13820
FTSJ1 Knockout jurkat Polyclonal Cells
Cat. No. ARG13741
HERPUD2 Knockout MES-OV Polyclonal Cells
Cat. No. ARG24527
ASH1L Knockout HAP1 Polyclonal Cells
Cat. No. ARG34708
MTM1 Knockout MES-OV Polyclonal Cells
Cat. No. ARG5989
The PRDX1 Knockout ACHN Cell Line is a CRISPR/Cas9-edited human knockout cell line in which the PRDX1 gene has been disrupted to eliminate peroxiredoxin-1 expression. This loss-of-function model is designed for studying the molecular contributions of PRDX1 to antioxidant defense, redox-sensitive signaling pathways, and disease-relevant processes. The cell line provides a genetically defined platform for functional assays and mechanistic investigations in a renal epithelial adenocarcinoma context, without explicit claims of monoclonality or specific editing patterns. It is suitable for advanced research applications in cancer biology, oxidative stress, and signal transduction.
The host ACHN cell line originates from the pleural effusion of a 22-year-old male with renal cell adenocarcinoma and displays epithelial, tumorigenic characteristics. ACHN cells are widely utilized as a model for renal cancer studies, including metastatic progression and drug sensitivity profiling. This parental line??s kidney epithelial origin offers a pathophysiologically relevant setting for assessing the consequences of PRDX1 loss on tumor cell behavior and redox homeostasis.
PRDX1, an antioxidant peroxidase, reduces hydrogen peroxide and alkyl hydroperoxides, thereby regulating intracellular redox balance. It binds and inhibits ASK1, preventing JNK and p38 MAPK activation; oxidative stress causes PRDX1 oxidation and release of ASK1 to trigger downstream kinases. PRDX1 also modulates NF-??B through interaction with p65. Upstream transcription factors Nrf2 and FOXO3a control PRDX1 expression in response to oxidative stress and growth signals. Additional targets include PTEN, protected from oxidative inactivation by PRDX1, and cell cycle regulators such as cyclins.
In the ACHN renal adenocarcinoma model, loss of PRDX1 function is expected to elevate intracellular hydrogen peroxide levels, disrupting redox-sensitive signaling networks that control tumor cell fate. Enhanced ASK1/JNK/p38 signaling may shift the balance toward apoptosis, while altered NF-??B activity could affect inflammatory and survival gene programs. Such perturbations may influence drug resistance, proliferation capacity, and metastatic potential, making this knockout line a relevant system for exploring PRDX1??s context-dependent roles in kidney cancer pathophysiology.
Experimental applications include quantitative gene expression analysis by RT-qPCR, protein detection via Western blotting, and immunofluorescence to confirm knockout and assess signaling molecules. Functional assays can measure ROS accumulation, apoptosis induction with flow cytometry, and proliferation changes. Phospho-kinase arrays enable profiling of JNK, p38, and NF-??B pathway activation. The model is particularly valuable for oxidative stress biology, chemosensitivity studies, and inflammation-related cancer research. For additional technical details or ordering inquiries, please reach out to Ascent Research.
