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Abcc8 Knockout INS-1 Cell Line

Cat. No. ARG0459
Product Type:

Genome-edited Cells

Tissue Source:

Pancreas

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Short Description 🔒

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.

Product Details
Cell Engineering
Immortalization
Culture Conditions
Quality Control
Disclaimer

Product Details

Product Type:
Genome-edited Cells
Tissue Source:
Pancreas
Age:
666 days
Size/Quantity:
1 million
Shipping info:
Cryopreserved in vials and shipped on dry ice

Cell Engineering Information

Host Cell:
INS-1
Gene Name:
Abcc8
Gene Alias:
ATP binding cassette subfamily C member 8
Gene Identifier:
NCBI Gene ID 25559
Gene Species:
Rattus norvegicus (Rat)
Gene Type:
protein coding gene
Gene Family:
ATP-binding cassette sub-family C

Immortalization Information

No immortalization information available.

Culture Conditions

Temperature:
37°C
Atmosphere:
5% CO₂

Quality Control

Mycoplasma testing:
Negative for mycoplasma through PCR analysis
Sterility testing:
Daily monitoring confirms that the cells are free from bacterial, yeast, and fungal contamination.
Pathogens:
Cells tested negative for HIV-1, HBV, and HCV.

Disclaimer

Intended Use:
This product is intended for laboratory in vitro use only. It is not intended for diagnostic, therapeutic, or clinical applications.
Disclaimer:
Ascent Research endeavors to provide accurate and up-to-date product information. However, no warranties or representations are made regarding its completeness or reliability.
Usage:
By accepting this product, the customer acknowledges and agrees to assume all risks associated with its receipt, handling, storage, disposal, and use. This product is provided "AS IS".

Description 🔒

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.