Potassium Inwardly-Rectifying Channel, Subfamily J, Member 11 (KCNJ11) (C-Term) antibody

Details for Product No. ABIN350386
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Antigen
Synonyms kir6.2, Kir6.2, mBIR, BIR, HHF2, IKATP, KIR6.2, PHHI, TNDM3
Epitope
C-Term
(22), (22), (14), (9), (7), (1), (1), (1), (1), (1), (1), (1)
Reactivity
Human
(71), (57), (33), (28), (24), (12)
Host
Rabbit
(65), (14), (1)
Clonality
Polyclonal
Conjugate
Un-conjugated
(4), (4), (4), (2), (2), (2), (2), (2), (2), (2), (2), (2), (2), (2)
Application
Immunohistochemistry (IHC), Western Blotting (WB)
(62), (45), (20), (17), (17), (10), (10), (2)
Pubmed 5 references available
Quantity 100 µL
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Catalog No. ABIN350386
454.67 $
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Immunogen A synthetic peptide from the c-terminal region of human KCNJ11 (Kir6.2) conjugated to an immunogenic carrier protein was used as the antigen. The antigen shares 94% identity with rat and mouse sequence.
Specificity Specific for KCNJ11.
Purification Whole serum
Alternative Name KCNJ11
Background 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. Defects in KCNJ11 are the cause of familial hyperinsulinemic hypoglycemia type 2 (HHF2), also known as persistent hyperinsulinemic hypoglycemia of infancy (PPHI) or hyperinsulinism. HHF2 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.
Subcellular location: Membrane, Multi-pass membrane protein. Also known as: ATP-sensitive inward rectifier potassium channel 11, Potassium channel, inwardly rectifying subfamily J member 11, Inward rectifier K(+) channel Kir6.2, IKATP.
Application Notes A dilution of 1 : 300 to 1 : 2000 is recommended.
The optimal dilution should be determined by the end user.
Not yet tested in other applications.
Restrictions For Research Use only
Format Lyophilized
Reconstitution Reconstitute in 500 µL of sterile water. Centrifuge to remove any insoluble material.
Handling Advice Avoid freeze and thaw cycles.
Storage 4 °C/-20 °C
Storage Comment Maintain the lyophilised/reconstituted antibodies frozen at -20°C for long term storage and refrigerated at 2-8°C for a shorter term. When reconstituting, glycerol (1:1) may be added for an additional stability. Avoid freeze and thaw cycles.
Expiry Date 12 months
General Inagaki, Gonoi, Clement et al.: "Reconstitution of IKATP: an inward rectifier subunit plus the sulfonylurea receptor." in: Science (New York, N.Y.), Vol. 270, Issue 5239, pp. 1166-70, 1996 (PubMed).

Sakura, Wat, Horton et al.: "Sequence variations in the human Kir6.2 gene, a subunit of the beta-cell ATP-sensitive K-channel: no association with NIDDM in while Caucasian subjects or evidence of abnormal function when expressed in vitro." in: Diabetologia, Vol. 39, Issue 10, pp. 1233-6, 1997 (PubMed).

Meissner, Beinbrech, Mayatepek: "Congenital hyperinsulinism: molecular basis of a heterogeneous disease." in: Human mutation, Vol. 13, Issue 5, pp. 351-61, 1999 (PubMed).

Halushka, Fan, Bentley et al.: "Patterns of single-nucleotide polymorphisms in candidate genes for blood-pressure homeostasis." in: Nature genetics, Vol. 22, Issue 3, pp. 239-47, 1999 (PubMed).

Stanik, Gasperikova, Paskova et al.: "Prevalence of permanent neonatal diabetes in Slovakia and successful replacement of insulin with sulfonylurea therapy in KCNJ11 and ABCC8 mutation carriers." in: The Journal of clinical endocrinology and metabolism, Vol. 92, Issue 4, pp. 1276-82, 2007 (PubMed).

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