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.
Kdm3a Knockout CT26.WT Cell Line
Cat. No. ARG43931
NT5C3A Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG18047
HSPA4L Knockout A549 Polyclonal Cells
Cat. No. ARG33812
HDAC6 Knockout MCF7 Polyclonal Cells
Cat. No. ARG36439
EFNB1 Knockout HEK293T Polyclonal Cells
Cat. No. ARG40691
SERPINB2 Knockout SW480 Cell Line
Cat. No. ARG0774
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.
