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Rabbit Polyclonal Phospho-KIR6.2 (T224) antibody (STJ90722)
Supplier: St John’s Laboratory Ltd.
Recommended applications: WB, IHC, IF, ELISA
Recommended dilution: WB 1:500-1:2000; IHC 1:100-1:300; IF 1:200-1:1000; ELISA 1:5000;
Recommended protocols: check protocols
Click or hover above images to see image description for KIR6.2 (phospho Thr224) Polyclonal Antibody.
Check alternative names for the antibodyExpand
KCNJ11 antibody,|ATP sensitive inward rectifier potassium channel 11 antibody|Beta cell inward rectifier subunit antibody|BIR antibody|HHF 2 antibody|HHF2 antibody|IKATP antibody|Inward rectifier K(+) channel Kir6.2 antibody|Inwardly rectifying potassium channel KIR6.2 antibody|IRK 11 antibody|IRK11 antibody|KCNJ11 antibody|Kir 6.2 antibody|Kir6.2 antibody|MGC133230 antibody|PHHI antibody|Potassium channel inwardly rectifing subfamily J member 11 antibody|Potassium channel, inwardly rectifying subfamily J member 11 antibody|Potassium inwardly rectifying channel J11 antibody|TNDM 3 antibody|TNDM3 antibody|Anti-Kir6.2 antibody (ab79171)
SCBT cat No: sc-390104|sc-392198|sc-11228|sc-20809|sc-11226|
KIR6.2 (phospho Thr224) Polyclonal Antibody
|Catalogue No.|| |
Human, Mouse, Rat
Phospho-KIR6.2 (T224) Polyclonal Antibody detects endogenous levels of KIR6.2 protein only when phosphorylated at T224.
Synthesized phospho-peptide derived from KIR62 (phospho Thr224) at AA range 160-240
WB, IHC, IF, ELISA
|Recommended dilution|| |
WB 1:500-1:2000; IHC 1:100-1:300; IF 1:200-1:1000; ELISA 1:5000;
|Molecular weight|| |
KIR6.2 (phospho Thr224) Antibody was tube-contained. Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
KIR6.2 (phospho Thr224) Antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
-20 Celsius degree. Avoid repeated freeze/thaw cycles.
|Alternative antibody names|| |
ATP-sensitive inward rectifier potassium channel 11 antibody, IKATP antibody, Inward rectifier Kantibody, + antibody, channel Kir6.2 antibody, Potassium channel, inwardly rectifying subfamily J member 11 antibody
|Protein names|| |
ATP-sensitive inward rectifier potassium channel 11 , IKATP , Inward rectifier K, + , channel Kir6.2 , Potassium channel, inwardly rectifying subfamily J member 11
|Protein function|| |
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 (By similarity). 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.
|Involvement in disease|| |
Familial hyperinsulinemic hypoglycemia 2 (HHF2) [MIM:601820]: Most common cause of persistent hypoglycemia in infancy. Unless early and aggressive intervention is undertaken, brain damage from recurrent episodes of hypoglycemia may occur. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Diabetes mellitus, permanent neonatal (PNDM) [MIM:606176]: 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. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Transient neonatal diabetes mellitus 3 (TNDM3) [MIM:610582]: 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. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Note: Defects in KCNJ11 may contribute to non-insulin-dependent diabetes mellitus (NIDDM), also known as diabetes mellitus type 2.; Maturity-onset diabetes of the young 13 (MODY13) [MIM:616329]: A form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease. . Note: The disease is caused by mutations affecting the gene represented in this entry.
|Protein sequence and domain|| |
Belongs to the inward rectifier-type potassium channel (TC 1.A.2.1) family. KCNJ11 subfamily. [View classification]
|Protein post-translational modifications|| |
Phosphorylation by MAPK1 results in changes in channel gating that destabilize the closed states and reduce the ATP sensitivity.
|Protein cellular localization|| |
Membrane; Multi-pass membrane protein
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St John’s Laboratory Ltd.
|Product type|| |
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