In Stock Cell Lines
Homo sapiens (Human)
Heart
Adherent
The AGO2 Knockout AC16 Cell Line is a CRISPR/Cas9-edited knockout line derived from AC16 human ventricular cardiomyocytes, disrupting Argonaute 2 (AGO2), the catalytic core of the miRNA-induced silencing complex (RISC). AGO2 guides miRNA-directed mRNA cleavage or translational repression, interacting with Dicer, TRBP, and GW182, and is modulated by Akt and MAPK signaling. Its loss deregulates targets like CDKN1A, BCL2, and PTEN. Ideal for miRNA target identification (Ago2-CLIP) and cardiac disease modeling, including hypertrophy and arrhythmias.
CAMP Knockout HAP1 Polyclonal Cells
Cat. No. ARG22241
ETFDH Knockout SK-HEP-1 Polyclonal Cells
Cat. No. ARG15316
ACACA Knockout MES-OV Polyclonal Cells
Cat. No. ARG24013
KIF3A Knockout 786-O Polyclonal Cells
Cat. No. ARG25428
ATG2B Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG31241
DRAM2 Knockout jurkat Polyclonal Cells
Cat. No. ARG39773
The AGO2 Knockout AC16 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from AC16 human ventricular cardiomyocytes, engineered for loss-of-function studies of Argonaute 2 (AGO2). As the catalytic core of the miRNA-induced silencing complex (RISC), AGO2 is essential for miRNA-mediated gene silencing. This cell line provides a stable, gene-disrupted model to investigate miRNA-dependent regulatory mechanisms in a cardiac context.
AC16 is an immortalized human cardiomyocyte line that retains key characteristics of adult ventricular myocytes, including expression of cardiac markers and contractile proteins. Widely used in cardiovascular research, it enables reproducible studies of hypertrophy, electrophysiology, and metabolic stress responses, serving as an accurate host for dissecting cardiac miRNA pathways.
Molecularly, AGO2 guides RISC to complementary mRNA targets, facilitating endonucleolytic cleavage or translational repression. It interacts with Dicer and TRBP during RISC assembly and with GW182/TNRC6 to recruit silencing effectors. AGO2 function is regulated by upstream kinases such as Akt and MAPK, and by miRNAs including hsa-miR-107. Downstream, it post-transcriptionally controls expression of genes like CDKN1A, BCL2, and PTEN, linking it to cell proliferation and apoptosis networks.
In cardiac physiology, AGO2 is integral to miRNA-controlled processes spanning development, hypertrophy, and fibrotic remodeling. Knocking out AGO2 in AC16 cells ablates the canonical miRNA-silencing machinery, permitting direct examination of miRNA contributions to transcriptomic and proteomic shifts in cardiomyocytes. This makes the system ideal for modeling cardiac diseases like heart failure and arrhythmias, where AGO2 and miRNAs are frequently dysregulated.
Researchers can employ this knockout cell line for Ago2-CLIP and RIP to map miRNA-mRNA interactions, luciferase reporter assays for target validation, and RNA-seq for global expression profiling. Functional readouts with miRNA mimics or inhibitors??combined with viability, apoptosis, and hypertrophy assays??extend its utility to drug target discovery in cancer and viral infection biology. For further details, please reach out to Ascent Research.
