Rabbit Polyclonal GIRK2 antibody. N-terminal. Suitable for IHC-P and reacts with Human samples. Immunogen corresponding to Synthetic Peptide within Human KCNJ6.
pH: 7.4
Preservative: 0.099% Sodium azide
Constituents: 99% PBS
IHC-P | |
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Human | Tested |
Mouse | Predicted |
Rat | Predicted |
Cow | Predicted |
Dog | Predicted |
Gorilla | Predicted |
Hamster | Predicted |
Horse | Predicted |
Monkey | Predicted |
Orangutan | Predicted |
Pig | Predicted |
Species | Dilution info | Notes |
---|---|---|
Species Human | Dilution info 20 µg/mL | Notes Perform heat-mediated antigen retrieval before commencing with IHC staining protocol. |
Species | Dilution info | Notes |
---|---|---|
Species Mouse, Rat, Horse, Hamster, Cow, Dog, Pig, Monkey, Gorilla, Orangutan | Dilution info - | Notes - |
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This potassium channel may be involved in the regulation of insulin secretion by glucose and/or neurotransmitters acting through G-protein-coupled receptors. 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.
GIRK2, KATP2, KCNJ7, KCNJ6, G protein-activated inward rectifier potassium channel 2, GIRK-2, BIR1, Inward rectifier K(+) channel Kir3.2, KATP-2
Rabbit Polyclonal GIRK2 antibody. N-terminal. Suitable for IHC-P and reacts with Human samples. Immunogen corresponding to Synthetic Peptide within Human KCNJ6.
pH: 7.4
Preservative: 0.099% Sodium azide
Constituents: 99% PBS
BLAST analysis of the peptide immunogen showed no homology with other human proteins.
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GIRK2 also known as G protein-coupled inwardly-rectifying potassium channel 2 or KCNJ6 serves as an inward rectifier potassium channel. Mechanically GIRK2 regulates the flow of K+ ions into the cell when activated by G proteins influencing cellular excitability. GIRK2 has a molecular weight of approximately 48 kDa. This protein is expressed in various tissues including the brain heart and pancreas where it plays a role in modulating neuronal signaling and cardiac rhythm.
The GIRK2 channel contributes to maintaining resting membrane potentials and controlling neuronal excitability. GIRK2 forms heteromultimeric complexes with other GIRK subunits such as GIRK1 to fully function. These complexes are essential for the proper regulation of synaptic transmission and responsiveness to neurotransmitters particularly in areas of the brain like the cerebellum and hippocampus which are critical for cognitive and motor functions.
GIRK2 plays a significant role in the GABAergic neurotransmission and dopaminergic pathways. In the GABAergic pathway GIRK2 aids in mediating inhibitory signals by enhancing the hyperpolarization of neurons therefore dampening neurotransmission. In dopaminergic pathways GIRK2 interacts closely with dopamine receptors to modulate dopamine-induced potassium conductance impacting processes related to mood and reward. These interactions implicate GIRK2 in the regulation of important signaling pathways related to neuronal function and mood regulation.
GIRK2 has been implicated in neurological conditions like Parkinson's disease and epilepsy. Alterations in GIRK2 expression or function can disrupt normal neuronal signaling potentially contributing to the pathophysiology of these disorders. In Parkinson's disease the dopaminergic neurons involving GIRK2 and its interactions with dopamine receptors become affected leading to motor dysfunction. Similarly in epilepsy abnormal GIRK2 function may impair synaptic inhibition resulting in uncontrolled neuronal excitability.
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Immunohistochemical analysis of formalin-fixed, paraffin-embedded Human pancreas (islet) tissue labeling GIRK2 with ab219190 at 20 μg/ml.
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