Genome-edited Cells
Pancreas
The Abcc8 Knockout INS-1 Cell Line is a CRISPR/Cas9-edited knockout cell model targeting the SUR1 regulatory subunit of K_ATP channels in rat pancreatic beta-cells. SUR1 partners with Kir6.2 to govern glucose-stimulated insulin secretion, and its disruption leads to constitutive depolarization and unregulated insulin release, mirroring human congenital hyperinsulinism. This knockout line enables mechanistic studies of K_ATP channel signaling, insulin exocytosis, and metabolic sensing. Applications include electrophysiology, calcium imaging, and drug screening for insulin secretagogues, making it a valuable tool for diabetes and beta-cell function research.
CSNK2A1 Knockout jurkat Polyclonal Cells
Cat. No. ARG13622
HRAS Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG30765
DIO1 Knockout HAP1 Polyclonal Cells
Cat. No. ARG38764
NARF Knockout MES-OV Polyclonal Cells
Cat. No. ARG6281
COA4 Knockout Raji Polyclonal Cells
Cat. No. ARG1014
Mouse Olfactory Bulb Neuron Medium
Cat. No. ARM0628
The Abcc8 Knockout INS-1 Cell Line is a CRISPR/Cas9-edited rat insulinoma cell line with targeted disruption of the Abcc8 gene, encoding the SUR1 regulatory subunit of ATP-sensitive potassium (K_ATP) channels. This loss-of-function model eliminates SUR1 expression, enabling dissection of K_ATP channel-dependent mechanisms in pancreatic beta-cell function.
The parental INS-1 line derives from an X-ray-induced rat insulinoma and retains glucose-responsive insulin secretion, making it a well-established model for beta-cell physiology. Its homogeneity and proliferative capacity make it ideal for knockout studies of insulin secretion and beta-cell dysfunction.
Abcc8/SUR1 partners with KCNJ11/Kir6.2 to form K_ATP channels, which are regulated by intracellular ATP/ADP ratio, MgADP, PIP2, and sulfonylureas. Channel closure upon glucose metabolism causes depolarization, opening voltage-gated Ca2+ channels (Cav1.2/1.3) and triggering Ca2+ influx. This promotes SNARE-mediated exocytosis of insulin granules. SUR1 also interacts with EPAC2 and Syntaxin-1A, linking cAMP/PKA signaling to the secretory machinery.
Abcc8 knockout disrupts K_ATP channel regulation, causing constitutive depolarization, Ca2+ influx, and unregulated insulin secretion??mimicking congenital hyperinsulinism with ABCC8 loss-of-function mutations. This model enables study of hyperinsulinemic states and counter-regulatory pathways, and facilitates pharmacological profiling of insulin secretagogues independent of K_ATP channel activity.
Applications include glucose-stimulated insulin secretion assays, patch clamp electrophysiology, Ca2+ imaging, and western blotting for downstream targets. The line supports screening of sulfonylurea analogs, investigation of SNARE-mediated exocytosis, and metabolic flux analyses. For ordering and technical support, contact Ascent Research.
