Overview |
bs-2436R-FITC |
Kir6.2 (KCNJ11) Polyclonal Antibody, FITC Conjugated |
WB, FCM, IF(IHC-P), IF(IHC-F), IF(ICC) |
Human, Mouse, Rat |
Dog, Cow, Rabbit |
Specifications |
FITC |
Rabbit |
KLH conjugated synthetic peptide derived from human Kir62 |
301-390/390 |
Polyclonal |
IgG |
1ug/ul |
Purified by Protein A. |
Aqueous buffered solution containing 0.01M TBS (pH 7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
Store at -20°C. Aliquot into multiple vials to avoid repeated freeze-thaw cycles. |
Target |
3767 |
Q14654 |
Cell membrane |
ATP sensitive inward rectier potassium channel 11; Beta cell inward rectier subunit; mBIR; BIR; HHF 2; HHF2; IKATP; Inward rectier K+ channel Kir6.2; Inwardly rectying potassium channel KIR6.2; IRK 11; IRK11; KCNJ11; Kir 6.2; Kir6.2; MGC133230; PHHI; Potassium channel, inwardly rectying subfamily J member 11; Potassium inwardly rectying channel J11; TNDM 3; TNDM3; IRK11_HUMAN. |
Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses. The protein encoded by this gene is an integral membrane protein and inward-rectifier type potassium channel. The encoded protein, which has a greater tendency to allow potassium to flow into a cell rather than out of a cell, is controlled by G-proteins and is found associated with the sulfonylurea receptor SUR. Mutations in this gene are a cause of familial persistent hyperinsulinemic hypoglycemia of infancy (PHHI), an autosomal recessive disorder characterized by unregulated insulin secretion. Defects in this gene may also contribute to autosomal dominant non-insulin-dependent diabetes mellitus type II (NIDDM), transient neonatal diabetes mellitus type 3 (TNDM3), and permanent neonatal diabetes mellitus (PNDM). Multiple alternatively spliced transcript variants that encode different protein isoforms have been described for this gene. [provided by RefSeq] |
Application Dilution |
WB |
1:300-5000 |
FCM |
1:20-100 |
IF(IHC-P) |
1:50-200 |
IF(IHC-F) |
1:50-200 |
IF(ICC) |
1:50-200 |