Neonatal diabetes - The role of KCNJ11 (Kir6.2)
ATP-sensitive potassium (KATP) channels are inhibited by intracellular ATP and activated by MgADP. As a consequence, they couple the metabolic state of the cell to its electrical activity. In pancreatic β-cells KATP channels regulate glucose-dependent insulin secretion and are the target for sulphon...
Main Author: | Tammaro, P |
---|---|
Format: | Journal article |
Language: | English |
Published: |
2007
|
Similar Items
-
Functional analysis of six Kir6.2 (KCNJ11) mutations causing neonatal diabetes.
by: Girard, C, et al.
Published: (2006) -
Functional analysis of two Kir6.2 (KCNJ11) mutations, K170T and E322K, causing neonatal diabetes.
by: Tarasov, A, et al.
Published: (2007) -
An in-frame deletion in Kir6.2 (KCNJ11) causing neonatal diabetes reveals a site of interaction between Kir6.2 and SUR1.
by: Craig, T, et al.
Published: (2009) -
Kir6.2 mutations causing neonatal diabetes provide new insights into Kir6.2-SUR1 interactions.
by: Tammaro, P, et al.
Published: (2005) -
Mutations at the same residue (R50) of Kir6.2 (KCNJ11) that cause neonatal diabetes produce different functional effects.
by: Shimomura, K, et al.
Published: (2006)