SMC-491
Kir6.1 Antibody, Clone N366/60
Cannot supply to this region.
- SKU:
- SMC-491
- Additional Names:
- Kir6.1, KCNJ8, Kcnj8, Inward rectifier K(+) channel Kir6.1, Potassium channel inwardly rectifying subfamily J member 8, ATP-sensitive inward rectifier potassium channel 8, uKATP-1
- Application:
- IHC, WB, IF, ICC
- Concentration:
- 1 mg/ml
- Species Reactivity:
- Rat
- Purification:
- Protein G Purified
- Storage Conditions:
- -20[o]C
- Supplier:
- StressMarq Biosciences
- Host:
- Mouse
- Reactivities:
- Human, Mouse, Rat
- ABP:
- IMP-GEN-2015-06 < 10% Serum <100ml
- Buffer:
- PBS pH7.4, 50% glycerol, 0.1% sodium azide
- Immunogen:
- Fusion protein amino acids 306-424 (Cytoplasmic C-terminus) of rat Kir6.1
- Clone:
- N366/60 (Formerly sold as S366-60)
- Uniprot:
- Q63664
- Synonyms:
- ATP-sensitive inward rectifier potassium channel 8;inward rectifier K(+) channel Kir6.1;inwardly rectifier K(+) channel Kir6.1;Inwardly rectifying potassium channel gene, subfamily J-8 (ATP sensitive);Kir6.1;potassium channel, inwardly rectifying subfamily J member 8;potassium voltage-gated channel subfamily J member 8;uKATP-1;UKATP1
- Extra Details:
- Kir6.1, encoded by the KCNJ8 gene, is a member of the inwardly rectifying potassium (Kir) channel family, which plays a critical role in regulating membrane potential and cellular excitability. Unlike voltage-gated potassium channels, Kir channels preferentially allow potassium ions to flow into the cell, stabilizing the resting membrane potential and modulating neuronal responsiveness. Kir6.1 is a key subunit of ATP-sensitive potassium (K_ATP) channels, which couple cellular metabolic state to electrical activity. While Kir6.1 is predominantly expressed in cardiac and smooth muscle tissues-including fetal and adult hearts-it is also present in the brain, where it contributes to neurovascular coupling and neuronal protection under metabolic stress. In the nervous system, Kir6.1-containing K_ATP channels are activated during conditions of energy depletion, such as ischemia or oxidative stress, helping to hyperpolarize neurons and reduce excitotoxicity. Dysregulation of Kir6.1 function has been implicated in neurodegenerative diseases, including stroke, Alzheimer's disease, and Parkinson's disease, where impaired energy metabolism and ionic imbalance are central pathological features. Furthermore, mutations in KCNJ8 have been associated with J-wave syndromes and other channelopathies, highlighting the broader physiological importance of Kir6.1 in excitable tissues. As research into metabolic regulation and ion channel dysfunction in neurodegeneration advances, Kir6.1 is emerging as a promising target for therapeutic intervention aimed at preserving neuronal function and preventing cell death.
- Shipping Conditions:
- Blue Ice