Potassium inwardly-rectifying channel, subfamily J, member 3, also known as KCNJ3 or Kir3.1, is a human gene. 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 plays an important role in regulating heartbeat. It associates with three other G-protein-activated potassium channels to form a hetero-tetrameric pore-forming complex. KCNJ3 has been shown to interact with KCNJ5. G protein-coupled inwardly-rectifying potassium channel Inward-rectifier potassium ion channel GRCh38: Ensembl release 89: ENSG00000162989 - Ensembl, May 2017 GRCm38: Ensembl release 89: ENSMUSG00000026824 - Ensembl, May 2017 "Human PubMed Reference:". "Mouse PubMed Reference:". "Entrez Gene: KCNJ3 ...
Although it has been known for nearly 20 yr that PIP2 is required for activation of GIRK channels (Huang et al., 1998; Sui et al., 1998), the structural details of how the association of PIP2 with GIRK channels leads to channel activation remain poorly described. The initial crystal structures of Kir2.2 and GIRK2 channels provided snapshots of how PIP2 binds to Kir channels, implicating positively charged, basic amino acids in the tether helix, the M2 TMD, and the N-terminal domain in the binding of one PIP2 molecule (Hansen et al., 2011; Whorton and MacKinnon, 2011, 2013). Indeed, a comparison of the amino acids in the tether helix among different Kir channels reveals a high degree of conservation among these basic residues (Fig. S1 a). However, atomic resolution structures are static and lack the dynamic interactions of ligands associating with the channel and inducing gating conformations. In the current study, we combined functional studies with MD simulations to provide evidence for a ...
Tipepidine (INN) (brand names Asverin, Antupex, Asvelik, Asvex, Bitiodin, Cofdenin A, Hustel, Nodal, Sotal), also known as tipepidine hibenzate (JAN), is a synthetic, non-opioid antitussive and expectorant of the thiambutene class. It acts as an inhibitor of G protein-coupled inwardly-rectifying potassium channels (GIRKs). The drug was discovered in the 1950s, and was developed in Japan in 1959. It is used as the hibenzate and citrate salts. The usual dose is 20 mg every 4-6 hours.[citation needed] Possible side effects of tipepidine, especially in overdose, may include drowsiness, vertigo, delirium, disorientation, loss of consciousness, and confusion. Tipepidine has recently garnered interest as a potential psychiatric drug. It is being investigated in depression, obsessive-compulsive disorder, and attention-deficit hyperactivity disorder (ADHD). Through inhibition of GIRK channels, tipepidine increases dopamine levels in the nucleus accumbens, but without increasing locomotor activity or ...
1N9P: Structural Basis of Inward Rectification: Cytoplasmic Pore of the G Protein-Gated Inward Rectifier GIRK1 at 1.8 A Resolution
We measured the impact of genetic ablation of GIRK1, GIRK2 and GIRK3 in mice using established behavioral paradigms. Assays were chosen that would provide insight into the contribution of GIRK channels to activity, anxiety, muscle co-ordination, ataxia and reward-related behavior. We found that GIRK1−/− mice and GIRK2−/− mice often displayed robust and similar phenotypes, including elevated open-field activity, decreased anxiety-like behavior, decreased baclofen ataxia and increased operant responding for food.. Overall, GIRK2−/− mice exhibited the most pronounced phenotypes in this study. These observations are consistent with the view that GIRK2 contributes to channel formation in most neuron populations that exhibit a GIRK conductance (Cruz et al. 2004; Koyrakh et al. 2005; Luscher et al. 1997; Slesinger et al. 1997; Torrecilla et al. 2002). GIRK2−/− mice have displayed phenotypes in many behavioral tests. For example, GIRK2−/− mice displayed blunted behavioral responses ...
Previous data from our laboratory has indicated that there is a functional link between the β-adrenergic receptor signaling pathway and the G-protein inwardly rectifying potassium channel (GIRK1) in human breast cancer cell lines. We wanted to determine if GIRK channels were expressed in lung cancers and if a similar link exists in lung cancer. GIRK1-4 expression and levels were determined by reverse transcription polymerase chain reaction (RT-PCR) and real-time PCR. GIRK protein levels were determined by western blots and cell proliferation was determined by a 5-bromo-2-deoxyuridine (BrdU) assay. GIRK1 mRNA was expressed in three of six small cell lung cancer (SCLC) cell lines, and either GIRK2, 3 or 4 mRNA expression was detected in all six SCLC cell lines. Treatment of NCI-H69 with β2-adrenergic antagonist ICI 118,551 (100 μM) daily for seven days led to slight decreases of GIRK1 mRNA expression levels. Treatment of NCI-H69 with the β-adrenergic agonist isoproterenol (10 μM) decreased growth
TY - JOUR. T1 - Discovery, synthesis and characterization of a series of (1-alkyl-3-methyl-1H-pyrazol-5-yl)-2-(5-aryl-2H-tetrazol-2-yl)acetamides as novel GIRK1/2 potassium channel activators. AU - Sharma, Swagat. AU - Kozek, Krystian A.. AU - Abney, Kristopher K.. AU - Kumar, Sushil. AU - Gautam, Nagsen. AU - Alnouti, Yazen. AU - David Weaver, C.. AU - Hopkins, Corey R.. PY - 2019/3/15. Y1 - 2019/3/15. N2 - The present study describes the discovery and characterization of a series of 5-aryl-2H-tetrazol-3-ylacetamides as G protein-gated inwardly-rectifying potassium (GIRK) channels activators. Working from an initial hit discovered during a high-throughput screening campaign, we identified a tetrazole scaffold that shifts away from the previously reported urea-based scaffolds while remaining effective GIRK1/2 channel activators. In addition, we evaluated the compounds in Tier 1 DMPK assays and have identified a (3-methyl-1H-pyrazol-1-yl)tetrahydrothiophene-1,1-dioxide head group that imparts ...
G protein-gated inwardly-rectifying potassium ion channels (GIRK) mediate the postsynaptic inhibitory effect of many neurotransmitters and related drugs of abus...
View mouse Kcnj2 Chr11:111066164-111076821 with: phenotypes, sequences, polymorphisms, proteins, references, function, expression
View mouse Kcnj16 Chr11:110968033-111027968 with: phenotypes, sequences, polymorphisms, proteins, references, function, expression
Reaktivität: Fledermaus, Rind (Kuh), Hund and more. 88 verschiedene KCNJ1 Antikörper vergleichen. Alle direkt auf antikörper-online bestellbar!
TY - JOUR. T1 - Quantitative analysis of mammalian GIRK2 channel regulation by G proteins, the signaling lipid PIP2 and Na+ in a reconstituted system. AU - Wang, Weiwei. AU - Whorton, Matthew R.. AU - MacKinnon, Roderick. PY - 2014. Y1 - 2014. N2 - GIRK channels control spike frequency in atrial pacemaker cells and inhibitory potentials in neurons. By directly responding to G proteins, PIP2 and Na(+), GIRK is under the control of multiple signaling pathways. In this study, the mammalian GIRK2 channel has been purified and reconstituted in planar lipid membranes and effects of Gα, Gβγ, PIP2 and Na(+) analyzed. Gβγ and PIP2 must be present simultaneously to activate GIRK2. Na(+) is not essential but modulates the effect of Gβγ and PIP2 over physiological concentrations. Gαi1(GTPγS) has no effect, whereas Gαi1(GDP) closes the channel through removal of Gβγ. In the presence of Gβγ, GIRK2 opens as a function of PIP2 mole fraction with Hill coefficient 2.5 and an affinity that poises ...
KIR3.4 antibody (potassium inwardly-rectifying channel, subfamily J, member 5) for ICC/IF, IHC, WB. Anti-KIR3.4 pAb (GTX54780) is tested in Human, Mouse, Rat samples. 100% Ab-Assurance.
TY - JOUR. T1 - Epistatic interaction of CREB1 and KCNJ6 on rumination and negative emotionality. AU - Lazary, Judit. AU - Juhasz, Gabriella. AU - Anderson, Ian M.. AU - Jacob, Christian P.. AU - Nguyen, T. Trang. AU - Lesch, Klaus Peter. AU - Reif, Andreas. AU - Deakin, J. F.William. AU - Bagdy, Gyorgy. PY - 2011/1/1. Y1 - 2011/1/1. N2 - G protein-activated K+ channel 2 (GIRK2) and cAMP-response element binding protein (CREB1) are involved in synaptic plasticity and their genes have been implicated depression and memory processing. Excessive rumination is a core cognitive feature of depression which is also present in remission. High scores on the Ruminative Response Scale (RRS) questionnaire are predictive of relapse and recurrence. Since rumination involves memory, we tested the hypothesis that variation in the genes encoding GIRK2 (KCNJ6) and CREB1 mechanisms would influence RRS scores. GIRK2 and CREB1 polymorphisms were studied in two independent samples (n = 651 and n = 1174) from the ...
Nakamura A, Fujita M, Ono H, Hongo Y, Kanbara T, Ogawa K, Morioka Y, Nishiyori A, Shibasaki M, Mori T, Suzuki T, Sakaguchi G, Kato A, Hasegawa ...
TY - JOUR. T1 - Molecular basis of downregulation of G-protein -coupled inward rectifying k+ current (ik,ach) in chronic human atrial fibrillation decrease in GIRK4 mrna correlates with reduced IK,ACh and muscarinic receptor-mediated shortening of action potentials. AU - Dobrev, Dobromir. AU - Graf, E.. AU - Wettwer, E.. AU - Himmel, H. M.. AU - Hála, O.. AU - Doerfel, C.. AU - Christ, T.. AU - Schüler, S.. AU - Ravens, U.. PY - 2001/11/20. Y1 - 2001/11/20. N2 - Background - Clinical and experimental evidence suggest that the parasympathetic nervous system is involved in the pathogenesis of atrial fibrillation (AF). However, it is unclear whether changes in G-protein-coupled inward rectifying K+ current (IK,ACh) contribute to chronic AF. Methods and Results - In the present study, we used electrophysiological recordings and competitive reverse-transcription polymerase chain reaction to study changes in IK,ACh and the level of the IK,ACh GIRK4 subunit in isolated human atrial myocytes and the ...
If SDF-1 acts downstream via GIRK channels, one would predict a change in GnRH neuronal movement in the presence of TPN-Q in +MNC explants (endogenous SDF-1 in midline cells) and no effect in −MNC explants (express little or no endogenous SDF-1). As predicted, a significant decrease in cell speed (15%) was seen when GIRK channels were blocked by TPN-Q (100 nM) in +MNC explants, while no differences in speed were detected after TPN-Q application in NPE-MNC explants (Table 4). These data are consistent with SDF-1 acting via GIRK channels to alter cell movement.. To further test if SDF signaling activates GIRK channels, −MNC explants were analyzed pre- and post-application of SDF-1 or SDF-1+TPN-Q. There was a significant decrease in TDS (23%) when TPN-Q was added with SDF-1, as compared to SDF-1 alone (Table 4; Fig. 3L), but these values were similar to the speed in the control condition (SFM, P,0.05). These data support the hypothesis that SDF-1/CXCR4-mediated movement is signaled via GIRK ...
HEK293-HuCACNA1C/NEUROD1/CACNA2D1/KCNJ2 cell line is a hypotriploid human cell line, which has been transfected with a human calcium channel, voltage-dependent, L type, alpha 1C subunit (CACNA1C), a human neuronal differentiation 1 (NEUROD1), a human calcium channel, voltage-dependent, alpha 2/delta subunit 1 (CACNA2D1) and a human potassium inwardly-rectifying channel, subfamily J, member 2 (KCNJ2) to allow stably express of the human CACNA1C, NEUROD1, CACNA2D1 and KCNJ2. It is an example of a cell line tr
A number of studies have been performed to identify the association between potassium inwardly-rectifying channel, subfamily J, member 11 (KCNJ11) gene and type 2 diabetes mellitus (T2DM) in East Asia
Ara, Cengiz; Çoban, Sacid; Işık, Burak; Özcan, Canan Ceran; Yılmaz, Sezai (Ulus Travma Acil Cerrahi Derg 2010;16 (3):275-276., 2010) ...
Weaver mice have a severe hypoplasia of the cerebellum with an almost complete loss of the midline granule cells. Recent genetic studies of weaver mice have identified a mutation resulting in an amino acid substitution (G156S) in the pore of the inwardly rectifying potassium channel subunit Kir 3.2. When expressed in Xenopus oocytes the weaver mutation alters channel selectivity from a potassium-selective to a nonspecific cation-selective pore. In this study we confirm by cell-attached patch-clamp recording that the mutation produces a non-selective cation channel. We also demonstrate that the cell death induced by weaver expression may be prevented by elimination of calcium from the extracellular solution as well as by coexpression with the wild-type Kir 3.2 allele, or other members of the Kir 3.0 subfamily. These results suggest that the weaver defect in Kir 3.2 may cause cerebellar cell death by cell swelling and calcium overload. Cells which express the weaver subunit, but which normally survive,
In the present study, we conducted: (i) in situ hybridization in order to investigate the expression of kainate and GABA(A) receptor subunits and the pre-proenkephalin and prodynorphin peptides in the brain of weaver mouse (a genetic model of dopamine deficiency) and (ii) immunocytochemistry in order to study the somatostatin-positive cells in weaver striatum. Our results indicated: (i) increases in mRNA levels of KA2 and GluR6 kainate receptor subunits, of alpha(4) and beta(3) GABA(A) receptor subunits and of pre-proenkephalin and prodynorphin in 6-month-old weaver striatum; (ii) a decrease in alpha(1) and beta(2) GABA(A) subunit mRNAs in 6-month-old weaver globus pallidus; (iii) increases in KA2, alpha(4) and beta(3) and decreases in alpha(2) and beta(2) mRNAs in the 6-month-old weaver somatosensory cortex; and (iv) an increase in somatostatin-immunopositive cells in 3-month-old weaver striatum. We suggest that: (i) in striatum, the alterations are induced by the induction of the transcription ...
Overexpression the KCNJ3, a gene that encodes subunit 1 of G-protein activated inwardly rectifying K+ channel (GIRK1) in the primary tumor has been found to be associated with reduced survival times and increased lymph node metastasis in breast cancer patients. In order to survey possible tumorigenic properties of GIRK1 overexpression, a range of malignant mammary epithelial cells, based on the MCF-7 cell line that permanently overexpress different splice variants of the KCNJ3 gene (GIRK1a, GIRK1c, GIRK1d and as a control, eYFP) were produced. Subsequently, selected cardinal neoplasia associated cellular parameters were assessed and compared. Adhesion to fibronectin coated surface as well as cell proliferation remained unaffected. Other vital parameters intimately linked to malignancy, i.e. wound healing, chemoinvasion, cellular velocities / motilities and angiogenesis were massively affected by GIRK1 overexpression. Overexpression of different GIRK1 splice variants exerted differential actions. While
Several inwardly-rectifying (Kir) potassium channels (Kin l 1, Kir41 and Kir4 2) are characterised by their sensitivity to inhibition by intracellular H+ within the physiological range The mechanism by which these channels are regulated by intracellular pH has been the subject of intense scrutiny for over a decade, yet the molecular identity of the titratable pH-sensor remains elusive In this study we have taken advantage of the acidic intracellular environment of S cerevisiae and used a K+-auxotrophic strain to screen for mutants of Kin 1 1 with impaired pH-sensitivity In addition to the previously identified K80M mutation, this unbiased screening approach identified a novel mutation (S172T) in the second transmembrane domain (TM2) that also produces a marked reduction in pH-sensitivity through destabilization of the closed-state However, despite this extensive mutagenic approach, no mutations could be identified which removed channel pH-sensitivity or which were likely to act as a separate H+-sensor
Gene Information 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. It associates with another G-protein-activated potassium channel to form a heteromultimeric pore-forming complex. [provided by RefSeq Jul 2008]. ...
KCNJ4 - KCNJ4 (Myc-DDK-tagged)-Human potassium inwardly-rectifying channel, subfamily J, member 4 (KCNJ4), transcript variant 2 available for purchase from OriGene - Your Gene Company.
KCNJ6 - KCNJ6 (Myc-DDK-tagged)-Human potassium inwardly-rectifying channel, subfamily J, member 6 (KCNJ6) available for purchase from OriGene - Your Gene Company.
Author(s): Stern, Kalyn Michiko | Abstract: Drug sensitization is thought to arise through changes in transcription, modification of signaling, and synaptic transmission. A novel rat gene, mrt1, may contribute to this neuronal plasticity as it is upregulated during sensitization. Mrt1 contains a PX domain which classifies it as a sorting nexins- thus mrt1 is also called SNX27. In addition, SNX27 also has a PDZ domain which has been demonstrated to interact with and mediate GIRK channel trafficking. To explore this interaction and the role that SNX27 may play in sensitization it is necessary to localize SNX27 expression. Using a novel SNX27 antibody I had three aims for my Masters project. First, to characterize the specificity of the antibody. Second, to characterize SNX27 expression in the brain, particularly in the hippocampus. Third, to correlate this expression back to an interaction with GIRK channels. The SNX27 antibody demonstrated good specificity for SNX27 protein. SNX27 was found to be
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Purpose: The inwardly-rectifying potassium channel Kir7.1 is present in the apical processes of retinal pigment epithelial (RPE) cells. Several mutations in the gene that encodes Kir7.1 (KCNJ13) cause blindness in the allelic disorders of Snowflake Vitreoretinal Degeneration (SVD) and Lebers Congenital Amaurosis (LCA16). In this study, we treated two Kir7.1 nonsense mutations that result in LCA16 (W53X and R166X) with the read-through compounds Ataluren (PTC-124; AdooQ Biosciences) and a novel small molecule, RTC-14.. Methods: Chinese Hamster Ovary (CHO-K1) cells were transfected with N-terminal GFP-fused W53X and R166X mutant plasmids. The cells were then treated with two different concentrations, 5 µM and 10 µM, of the read-through compounds PTC-124 or RTC-14 after eight hours of transfection, and the cells were incubated with these drugs for 36 hours. Whole-cell patch clamp electrophysiology was performed on the transfected cells. Function of the Kir7.1 channel was measured in the presence ...
Berlin, S., Hadad, E., Heled, Y., and Moran, D.S. (2004). The Efficacy of Nutritional Supplements upon Physical Exercise. Journal of Israeli Military Medicine 1(2), 72-80.. Berlin, S., Shalit, L., Yarom, Y., and Moran, D.S. (2007). Metabolic rate prediction by massless actigraphy for outdoor activities. Mil Med 172, 882-887.. Eliyahu, U., Berlin, S., Hadad, E., Heled, Y., and Moran, D.S. (2007). Psychostimulants and military operations. Mil Med 172, 383-387.. Rubinstein, M., Peleg, S., Berlin, S., Brass, D., and Dascal, N. (2007). Galphai3 primes the G protein-activated K+ channels for activation by coexpressed Gbetagamma in intact Xenopus oocytes. J Physiol 581, 17-32.. Berlin S. (2009). Do bigger and "better" labs have easier access to high impact factor journals? Science signaling. December 9th, E-letter. http://stke.sciencemag.org/content/2/99/eg15.e-letters (Addition to Living by The Numbers- Michael B. Yaffe; 01 Dec 2009: Vol. 2, Issue 99, pp. eg15, doi: 10.1126/scisignal.299eg15).. Lvov, ...
Discover Earl Weaver famous and rare quotes. Share Earl Weaver quotations about baseball, sports and winning. The key to winning baseball games is pitching...
Eagles fullback Leonard Weaver has become among the first players to publicly weigh in on the McNabb trade situation. - Daily News staff, Philadelphia Daily News
Roboticists have begun to design biologically inspired robots with soft or partially soft bodies, which have the potential to be more robust and adaptable, and safer for human interaction, than traditional rigid robots ...
Acid reflux from having steak might cause acne, also. Much like dairy food, your body has difficulty digesting steak. Your body works so difficult to break across the various meats it cant successfully eradicate other toxic compounds, making those to be released with the epidermis and resulting in acne breakouts. You dont need to go vegan, but keep to the quickly consumed white colored meat and fish to additional your epidermis additional misuse. [url=http://www.x21w12w21.info]Folii9000[/url ...
Bladder cancer (BC) is the ninth most common cancer and the 13th most common cause of cancer death. Although p21 protein-activated kinase (PAK) regulates cell growth, motility, and morphology, the...
Weaver silver cross lock scope rings ensure secure and tight fit on riflescopes. Shop these tested grand slam steel rings for great shooting performance.
https://www.nationalgeographic.com/photography/photo-of-the-day/2011/1/southern-masked-weaver.html © 1996-2015 National Geographic Society, © 2015- 2019 National Geographic Partners, LLC. All rights reserved ...
Aldosterone-producing adenomas (APAs) cause a sporadic form of primary aldosteronism and somatic mutations in the KCNJ5 gene, which encodes the G-protein-activated inward rectifier K+ channel 4, GIRK4, account for ≈40% of APAs. Additional somatic APA mutations were identified recently in 2 other genes, ATP1A1 and ATP2B3, encoding Na+/K+-ATPase 1 and Ca2+-ATPase 3, respectively, at a combined prevalence of 6.8%. We have screened 112 APAs for mutations in known hotspots for genetic alterations associated with primary aldosteronism. Somatic mutations in ATP1A1, ATP2B3, and KCNJ5 were present in 6.3%, 0.9%, and 39.3% of APAs, respectively, and included 2 novel mutations (Na+/K+-ATPase p.Gly99Arg and GIRK4 p.Trp126Arg). CYP11B2 gene expression was higher in APAs harboring ATP1A1 and ATP2B3 mutations compared with those without these or KCNJ5 mutations. Overexpression of Na+/K+-ATPase p.Gly99Arg and GIRK4 p.Trp126Arg in HAC15 adrenal cells resulted in upregulation of CYP11B2 gene expression and its ...
A channel that is "inwardly-rectifying" is one that passes current (positive charge) more easily in the inward direction (into the cell) than in the outward direction (out of the cell). It is thought that this current may play an important role in regulating neuronal activity, by helping to stabilize the resting membrane potential of the cell. By convention, inward current (positive charge moving into the cell) is displayed in voltage clamp as a downward deflection, while an outward current (positive charge moving out of the cell) is shown as an upward deflection. At membrane potentials negative to potassiums reversal potential, inwardly rectifying K+ channels support the flow of positively charged K+ ions into the cell, pushing the membrane potential back to the resting potential. This can be seen in figure 1: when the membrane potential is clamped negative to the channels resting potential (e.g. -60 mV), inward current flows (i.e. positive charge flows into the cell). However, when the ...
Research Grant Recipient: Jennifer Westendorf, PhD. Award Value: $250,000. Research Focus: Osteoarthritis. Project Summary: This project will help determine how proteins called Girk2 and Girk3 contribute to cartilage formation and repair in the setting of osteoarthritis. The investigators believe that osteoarthritis can be prevented if these proteins are absent or inactive. This work will lead to the development of better strategies to treat osteoarthritis.. Dr. Westendorf studies the molecular the epigenetic basis for skeltal formation, the regeneration of bone and cartilage, and the growth of pirmary and metastatic bone tumors. She is the vice chair of the Department of Biochemistry and Molecular Biology, and a consultant for the Department of Orthopedic Surgery at Mayo Clinic.. ...
DCAT: At the organizations annual membership meeting DCAT installed Dix Weaver, Sr. supply chain consultant at Eli Lilly and company as the new president of the organization for 2008. Mr. Weaver succeeds Joe Colleluori, Lonza Inc. and is
Expression of KCNJ6 (BIR1, GIRK2, hiGIRK2, KATP2, KCNJ7, Kir3.2) in hippocampus tissue. Antibody staining with in immunohistochemistry.
Expression of KCNJ6 (BIR1, GIRK2, hiGIRK2, KATP2, KCNJ7, Kir3.2) in ovary tissue. Antibody staining with in immunohistochemistry.
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When it comes to pain, guys may be tougher than gals because they have more of a particular type of protein, new research suggests. Two studies published online this week by the Proceedings of the National Academy of Sciences implicate proteins known as GIRKs in sex-based differences in pain sensitivity in mice. The findings could help researchers develop new gender-specific treatments for discomfort. Previous research had shown that males tend to have a higher threshold for pain than females do and that medications affect the sexes differently, although the precise mechanism remained unclear. In the new work, scientists tested analgesic drugs on mice unable to produce the GIRK2 protein. Allan I. Basbaum of Rockefeller University and his colleagues found that male mutants had lower pain thresholds than normal male mice. Female mutants exhibited a tolerance comparable to that of their normal counterparts, however, suggesting that GIRK2 is responsible for sex differences in pain sensitivity. Male ...
A budget friendly kit of Kir channel antibodies from Alomone Labs, ideal for screening purposes. An economical way to sample Abs. Control antigens included. Lyophilized. Worldwide shipping at room temperature. Top supplier for inward rectifier K+ channel research! Join the thousands of researchers using our products.
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Mechanism of GIRK Activation. P2Y1 -mediated activation of IGIRK was PTX-sensitive and strongly inhibited by over-expressing the Gβγ-scavenging protein, Gα-transducin. This implies that-as for GIRK-activation by α2 adrenoceptors or M2 muscarinic receptors in these neurons (Ruiz-Velasco and Ikeda, 1998; Fernandez-Fernandez et al., 2001)-P2Y-induced activation is mediated by βγ-subunits liberated from stimulated Gi protein heterotrimers. This accords with the mechanism of GIRK activation by G protein-coupled receptors deduced from many other studies (see Wickman and Clapham, 1995; Stanfield et al., 2002).. Mechanism of GIRK Inhibition. In contrast, IGIRK inhibition by P2Y receptors is probably mediated by the α-subunit of Gq/11 because 1) it was attenuated by RGS2, which specifically interacts with Gαq/11 (Heximer et al., 1997), and 2) was unaffected by RGS11, which interacts with Gβq (see Results) (Lei et al., 2000, 2001). This corresponds with the most likely G protein-coupling required ...