Kir2.1 Antibody, Clone S112

Cannot supply to this region.

SKU:: SMC-310
Additional Names:: Kir2.1, KCNJ2, Inward rectifier potassium channel 2, Inward rectifier K(+) channel Kir2.1, Potassium channel inwardly rectifying subfamily J member 2, IRK1, HHBIRK1, HHIRK1, HIRK 1, LQT7, SQT3
Application:: IHC, WB, IF, ICC, Microarray
Concentration:: 1 mg/ml
Species Reactivity:: Mouse
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, 0.09% sodium azide
Immunogen:: Fusion protein amino acids 41-64 and 189-428 of mouse Kir2.1
Clone:: S112
Uniprot:: P35561
Synonyms:: inward rectifier K(+) channel Kir2.1;inward rectifier potassium channel 2;IR;IRK-1;IRK1;Kcnf;Kcnf1;Kir2;Kir2.1;potassium channel, inwardly rectifying subfamily J member 2
Extra Details:: Kir2.1, encoded by the KCNJ2 gene, is a member of the inward-rectifier potassium (Kir) channel family, which plays a critical role in stabilizing the resting membrane potential and regulating neuronal excitability. Unlike other potassium channels, Kir2.1 preferentially allows potassium influx over efflux, helping maintain hyperpolarized membrane states essential for proper neuronal signaling. While Kir2.1 is well-characterized in cardiac and skeletal muscle-where mutations in KCNJ2 are linked to Andersen-Tawil syndrome-its role in the central nervous system is gaining increasing attention. Kir2.1 is expressed in various brain regions, where it contributes to the fine-tuning of synaptic transmission, action potential threshold, and excitatory-inhibitory balance. Disruption of Kir2.1 function has been implicated in neurological and neurodegenerative disorders, including epilepsy, Parkinson's disease, and Alzheimer's disease. Altered Kir2.1 activity can lead to aberrant neuronal firing, increased susceptibility to excitotoxicity, and impaired neuroplasticity-key mechanisms underlying neurodegeneration. Furthermore, Kir2.1 interacts with signaling pathways and scaffolding proteins that influence synaptic architecture and neuronal survival. Its pharmacological modulation presents a potential therapeutic avenue for restoring electrical homeostasis in diseased neural circuits. As research into ion channelopathies expands, Kir2.1 is emerging as a critical target in the study of neurodegenerative disease mechanisms and the development of neuroprotective strategies.

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