NP_112648.2
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NCBI GenBank Nucleotide #
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UniProt Primary Accession #
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UniProt Secondary Accession #
UniProt Related Accession #
Molecular Weight
43,608 Da
NCBI Official Full Name
ATP-sensitive inward rectifier potassium channel 11
NCBI Official Synonym Full Names
potassium voltage-gated channel subfamily J member 11
NCBI Official Synonym Symbols
NCBI Protein Information
ATP-sensitive inward rectifier potassium channel 11
UniProt Protein Name
ATP-sensitive inward rectifier potassium channel 11
UniProt Synonym Protein Names
BIR; Inward rectifier K(+) channel Kir6.2; Potassium channel, inwardly rectifying subfamily J member 11
UniProt Entry Name
KCJ11_RAT
NCBI Summary for Kcnj11
an ATP-sensitive K+ channel [RGD, Feb 2006]
UniProt Comments for Kcnj11
Kir6.2: This receptor is controlled by G proteins. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by extracellular barium. Subunit of ATP-sensitive potassium channels (KATP). Can form cardiac and smooth muscle-type KATP channels with ABCC9. KCNJ11 forms the channel pore while ABCC9 is required for activation and regulation. Defects in KCNJ11 are the cause of familial hyperinsulinemic hypoglycemia type 2 (HHF2); also known as persistent hyperinsulinemic hypoglycemia of infancy (PPHI) or congenital hyperinsulinism. HHF is the most common cause of persistent hypoglycemia in infancy and is due to defective negative feedback regulation of insulin secretion by low glucose levels. It causes nesidioblastosis, a diffuse abnormality of the pancreas in which there is extensive, often disorganized formation of new islets. Unless early and aggressive intervention is undertaken, brain damage from recurrent episodes of hypoglycemia may occur. Defects in KCNJ11 are a cause of diabetes mellitus permanent neonatal (PNDM). PNDM is a rare form of diabetes distinct from childhood-onset autoimmune diabetes mellitus type 1. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life. Permanent neonatal diabetes requires lifelong therapy. Defects in KCNJ11 are the cause of transient neonatal diabetes mellitus type 3 (TNDM3). Neonatal diabetes mellitus, defined as insulin-requiring hyperglycemia within the first month of life, is a rare entity. In about half of the neonates, diabetes is transient and resolves at a median age of 3 months, whereas the rest have a permanent form of diabetes. In a significant number of patients with transient neonatal diabetes mellitus, diabetes type 2 appears later in life. The onset and severity of TNDM3 is variable with childhood-onset diabetes, gestational diabetes or adult-onset diabetes described. Defects in KCNJ11 may contribute to non-insulin- dependent diabetes mellitus (NIDDM), also known as diabetes mellitus type 2. Belongs to the inward rectifier-type potassium channel (TC 1.A.2.1) family. KCNJ11 subfamily.
Protein type: Membrane protein, integral; Membrane protein, multi-pass; Channel, potassium
Research Articles on Kcnj11
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Products associated with Kcnj11 recombinant protein
Pathways associated with Kcnj11 recombinant protein
Diseases associated with Kcnj11 recombinant protein
Organs/Tissues associated with Kcnj11 recombinant protein
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