mProX™ Human KCNJ11 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Ion Channel Cell Lines
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Published Data
Fig.1 Specific deletion of the Kcnj11 gene in β cells (βKcnj11-/-) severely impairs glucose tolerance and GIIS in mice.
The electrophysiology of Kcnj11fl/fl and βKcnj11-/- mice's β cells. On the left, you can see an example of whole-cell KATP current recordings in primary β cells that were separated from Kcnj11fl/fl and βKcnj11-/- mice. Conductance adjusted to cell capacitance is in the middle. The perforated patch was used to evaluate the resting membrane potential of primary β cells from both control and βKcnj11-/- mice.
Ref: Oduori, Okechi S., et al. "Gs/Gq signaling switch in β cells defines incretin effectiveness in diabetes." The Journal of clinical investigation 130.12 (2020): 6639-6655.
Pubmed: 33196462
DOI: 10.1172/JCI140046
Research Highlights
In pancreatic beta cells, the ATP-sensitive potassium (KATP) channel mediates insulin secretion. This channel is a heteromeric protein made up of sulfonylurea receptor 1 subunits surrounding the pore and four inward-rectifier potassium ion channel (Kir6.2) tetramers, which constitute the KATP channel's pore.
Haghvirdizadeh, Polin, et al. "KCNJ11: genetic polymorphisms and risk of diabetes mellitus." Journal of diabetes research 2015 (2015).
Pubmed:
26448950
DOI:
10.1155/2015/908152
Research has demonstrated a correlation between mutations in the KCNJ11 gene and the following conditions: hyperinsulinemic hypoglycemia, type 2 diabetes mellitus (T2DM), maturity-onset diabetes of the young 13 (MODY13), and newborn diabetes mellitus (NDM).
He, Binbin, Xia Li, and Zhiguang Zhou. "Continuous spectrum of glucose dysmetabolism due to the KCNJ11 gene mutation-Case reports and review of the literature." Journal of Diabetes 13.1 (2021): 19-32.
Pubmed:
32935446
DOI:
10.1111/1753-0407.13114