P8122
Anti-Potassium Channel KIR3.2 (GIRK2) antibody produced in rabbit
affinity isolated antibody, lyophilized powder
Synonym(s):
Anti-BIR1, Anti-GIRK-2, Anti-GIRK2, Anti-KATP-2, Anti-KATP2, Anti-KCNJ7, Anti-KIR3.2, Anti-KPLBS, Anti-hiGIRK2
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About This Item
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biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
lyophilized powder
species reactivity
mouse, rat
technique(s)
western blot: 1:200 using rat brain membranes
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... KCNJ6(3763)
mouse ... Kcnj6(16522)
rat ... Kcnj6(25743)
General description
G protein-activated inward rectifier potassium channel 2 (GIRK2) is localized on the plasma membrane. It is expressed majorly in the brain and to some extent in the pancreas. The GIRK2 gene is mapped to human chromosome 21q22.13. Structurally, GIRK2 exists as a tetramer and comprises a transmembrane domain and a cytoplasmic domain.
Specificity
Anti-Potassium Channel KIR3.2 (GIRK2) recognizesKIR3.2 (GIRK2).
Immunogen
GST fusion protein with sequence corresponding to residues 374-414 of mouse KIR3.2 (GIRK2). Sequence homology is 40/41, 39/41, and 37/41 residues identical in rat, golden hamster, and human, respectively.
Application
Biochem/physiol Actions
G protein-activated inward rectifier potassium channel 2,(GIRK2) plays a key role in γ-aminobutyric acid-ergic (GABAergic), dopaminergic, cholinergic, and glutamatergic synapses. It also regulates neuronal excitability. GIRK2 through G protein-coupled receptor stimulation modulates neuronal circuit activity and heart rate in cardiac cells. Deletion of the GIRK2 gene in mice may lead to an anxiety-like phenotype and a depression-resistant behavior.
Physical form
Lyophilized powder from phosphate buffered saline containing 1% bovine serum albumin and 0.05% sodium azide.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class Code
13 - Non Combustible Solids
WGK
WGK 2
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
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Nerea Llamosas et al.
The international journal of neuropsychopharmacology, 18(11), pyv051-pyv051 (2015-05-10)
Targeting dorsal raphe 5-HT1A receptors, which are coupled to G-protein inwardly rectifying potassium (GIRK) channels, has revealed their contribution not only to behavioral and functional aspects of depression but also to the clinical response to its treatment. Although GIRK channels
Chella Kamarajan et al.
International journal of psychophysiology : official journal of the International Organization of Psychophysiology, 115, 13-23 (2016-12-21)
Event related oscillations (EROs) are heritable measures of neurocognitive function that have served as useful phenotype in genetic research. A recent family genome-wide association study (GWAS) by the Collaborative Study on the Genetics of Alcoholism (COGA) found that theta EROs
Matthew R Whorton et al.
Cell, 147(1), 199-208 (2011-10-04)
G protein-gated K(+) channels (Kir3.1-Kir3.4) control electrical excitability in many different cells. Among their functions relevant to human physiology and disease, they regulate the heart rate and govern a wide range of neuronal activities. Here, we present the first crystal
S Kumar et al.
Anaesthesia, 74(11), 1456-1470 (2019-08-28)
Advances in the field of pharmacogenomics have resulted in the discovery of some important single-nucleotide polymorphisms which are found to be associated with opioid dose variability. This, to a large extent, explains genetic variability in the analgesic dose of opioids.
Carlo Corona et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 38(27), 6102-6113 (2018-06-08)
Activating Transcription Factor 4 (ATF4) has been postulated as a key regulator of learning and memory. We previously reported that specific hippocampal ATF4 downregulation causes deficits in synaptic plasticity and memory and reduction of glutamatergic functionality. Here we extend our
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