Target Information

General Information of This Target
Target ID
BTDT00225
Target Name
G protein-activated inward rectifier potassium channel 1 (Kcnj3);G protein-activated inward rectifier potassium channel 2 (Kcnj6)
Target Bioclass
Transporter and channel
Uniprot ID
P63250 ; P48542
3D Structure
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2D Sequence
3D Structure
Source
Predict by Alphafold2
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Alphafold Parameters: msa_mode: mmseqs2_uniref_env model_type: auto num_recycles: auto
Gene Name
Kcnj3;Kcnj6
Gene ID
16519 ; 16522
Synonym 1
Inward rectifier K(+) channel Kir3.1; Potassium channel, inwardly rectifying subfamily J member 3
Synonym 2
Inward rectifier K(+) channel Kir3.2; Potassium channel, inwardly rectifying subfamily J member 6
Sequence 1
MSALRRKFGDDYQVVTTSSSGSGLQPQGPGQGPQQQLVPKKKRQRFVDKNGRCNVQHGNL
GSETSRYLSDLFTTLVDLKWRWNLFIFILTYTVAWLFMASMWWVIAYTRGDLNKAHVGNY
TPCVANVYNFPSAFLFFIETEATIGYGYRYITDKCPEGIILFLFQSILGSIVDAFLIGCM
FIKMSQPKKRAETLMFSEHAVISMRDGKLTLMFRVGNLRNSHMVSAQIRCKLLKSRQTPE
GEFLPLDQLELDVGFSTGADQLFLVSPLTICHVIDAKSPFYDLSQRSMQTEQFEVVVILE
GIVETTGMTCQARTSYTEDEVLWGHRFFPVISLEEGFFKVDYSQFHATFEVPTPPYSVKE
QEEMLLMSSPLIAPAITNSKERHNSVECLDGLDDISTKLPSKLQKITGREDFPKKLLRMS
STTSEKAYSLGDLPMKLQRISSVPGNSEEKLVSKTTKMLSDPMSQSVADLPPKLQKMAGG
PTRMEGNLPAKLRKMNSDRFT

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Sequence 2
MTMAKLTESMTNVLEGDSMDQDVESPVAIHQPKLPKQARDDLPRHISRDRTKRKIQRYVR
KDGKCNVHHGNVRETYRYLTDIFTTLVDLKWRFNLLIFVMVYTVTWLFFGMIWWLIAYIR
GDMDHIEDPSWTPCVTNLNGFVSAFLFSIETETTIGYGYRVITDKCPEGIILLLIQSVLG
SIVNAFMVGCMFVKISQPKKRAETLVFSTHAVISMRDGKLCLMFRVGDLRNSHIVEASIR
AKLIKSKQTSEGEFIPLNQSDINVGYYTGDDRLFLVSPLIISHEINQQSPFWEISKAQLP
KEELEIVVILEGIVEATGMTCQARSSYITSEILWGYRFTPVLTMEDGFYEVDYNSFHETY
ETSTPSLSAKELAELANRAEVPLSWSVSSKLNQHAELETEEEEKNPEELTERNGDVANLE
NESKV

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Family1
the inward rectifier-type potassium channel (TC 1.A.2.1) family.
Family2
the inward rectifier-type potassium channel (TC 1.A.2.1) family
Function 1
This potassium channel is controlled by G proteins. 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. This receptor plays a crucial role in regulating; the heartbeat.

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Function 2
This potassium channel is controlled by G proteins. It plays; a role in granule cell differentiation, possibly via membrane; hyperpolarization. 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.

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Taxonomy ID
10090
TCDB ID
. ; .
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Kingdom: Metazoa
Phylum: Chordata
Class: Mammalia
Order: Rodentia
Family: Muridae
Genus: Mus
Species: Mus musculus
Toxin Information Related to This Target
                           Toxin Name Activity Data Type Activity Data Reference
 Toxin Info    Apamin Inhibition rate . [1- 18]
 Toxin Info    U-actitoxin-Avd3n Effective concentration 50
80.9 μM
 [19]
References
Ref 1 The precursors of the bee venom constituents apamin and MCD peptide are encoded by two genes in tandem which share the same 3'-exon. J Biol Chem. 1995 May 26;270(21):12704-8. doi: 10.1074/jbc.270.21.12704.
Ref 2 The peptide components of bee venom. Eur J Biochem. 1976 Jan 15;61(2):369-76. doi: 10.1111/j.1432-1033.1976.tb10030.x.
Ref 3 Apamin as a selective blocker of the calcium-dependent potassium channel in neuroblastoma cells: voltage-clamp and biochemical characterization of the toxin receptor. Proc Natl Acad Sci U S A. 1982 Feb;79(4):1308-12. doi: 10.1073/pnas.79.4.1308.
Ref 4 Apamin, a blocker of the calcium-activated potassium channel, induces neurodegeneration of Purkinje cells exclusively. Brain Res. 1997 Dec 19;778(2):405-8. doi: 10.1016/s0006-8993(97)01165-7.
Ref 5 Determinants of apamin and d-tubocurarine block in SK potassium channels. J Biol Chem. 1997 Sep 12;272(37):23195-200. doi: 10.1074/jbc.272.37.23195.
Ref 6 Pharmacological characterization of small-conductance Ca(2+)-activated K(+) channels stably expressed in HEK 293 cells. Br J Pharmacol. 2000 Mar;129(5):991-9. doi: 10.1038/sj.bjp.0703120.
Ref 7 SK3 is an important component of K(+) channels mediating the afterhyperpolarization in cultured rat SCG neurones. J Physiol. 2001 Sep 1;535(Pt 2):323-34. doi: 10.1111/j.1469-7793.2001.00323.x.
Ref 8 Apamin interacts with all subtypes of cloned small-conductance Ca2+-activated K+ channels. Pflugers Arch. 2001 Jan;441(4):544-50. doi: 10.1007/s004240000447.
Ref 9 An amino acid outside the pore region influences apamin sensitivity in small conductance Ca2+-activated K+ channels. J Biol Chem. 2007 Feb 9;282(6):3478-86. doi: 10.1074/jbc.M607213200. Epub 2006 Dec 1.
Ref 10 Apamin reduces neuromuscular transmission by activating inhibitory muscarinic M(2) receptors on motor nerve terminals. Eur J Pharmacol. 2010 Jan 25;626(2-3):239-43. doi: 10.1016/j.ejphar.2009.09.064. Epub 2009 Oct 8.
Ref 11 Allosteric block of KCa2 channels by apamin. J Biol Chem. 2010 Aug 27;285(35):27067-27077. doi: 10.1074/jbc.M110.110072. Epub 2010 Jun 18.
Ref 12 The small neurotoxin apamin blocks not only small conductance Ca(2+) activated K(+) channels (SK type) but also the voltage dependent Kv1.3 channel. Eur Biophys J. 2017 Sep;46(6):517-523. doi: 10.1007/s00249-016-1196-0. Epub 2017 Jan 20.
Ref 13 Apamin inhibits TNF-- and IFN--induced inflammatory cytokines and chemokines via suppressions of NF-B signaling pathway and STAT in human keratinocytes. Pharmacol Rep. 2017 Oct;69(5):1030-1035. doi: 10.1016/j.pharep.2017.04.006. Epub 2017 Apr 18.
Ref 14 Apamin Suppresses LPS-Induced Neuroinflammatory Responses by Regulating SK Channels and TLR4-Mediated Signaling Pathways. Int J Mol Sci. 2020 Jun 17;21(12):4319. doi: 10.3390/ijms21124319.
Ref 15 Apamin from bee venom suppresses inflammation in a murine model of gouty arthritis. J Ethnopharmacol. 2020 Jul 15;257:112860. doi: 10.1016/j.jep.2020.112860. Epub 2020 Apr 11.
Ref 16 Antioxidative, Antiapoptotic, and Anti-Inflammatory Effects of Apamin in a Murine Model of Lipopolysaccharide-Induced Acute Kidney Injury. Molecules. 2020 Dec 3;25(23):5717. doi: 10.3390/molecules25235717.
Ref 17 Solution structure of apamin determined by nuclear magnetic resonance and distance geometry. Biochemistry. 1988 Nov 1;27(22):8491-8. doi: 10.1021/bi00422a029.
Ref 18 Binding and toxicity of apamin. Characterization of the active site. Eur J Biochem. 1991 Mar 28;196(3):639-45. doi: 10.1111/j.1432-1033.1991.tb15860.x.
Ref 19 AsKC11, a Kunitz Peptide from Anemonia sulcata, Is a Novel Activator of G Protein-Coupled Inward-Rectifier Potassium Channels. Mar Drugs. 2022 Feb 15;20(2):140. doi: 10.3390/md20020140.
Ref 20 Engineered specific and high-affinity inhibitor for a subtype of inward-rectifier K+ channels. Proc Natl Acad Sci U S A. 2008 Aug 5;105(31):10774-8. doi: 10.1073/pnas.0802850105. Epub 2008 Jul 31.
Ref 21 Structural Determinants Mediating Tertiapin Block of Neuronal Kir3.2 Channels. Biochemistry. 2020 Feb 25;59(7):836-850. doi: 10.1021/acs.biochem.9b01098. Epub 2020 Feb 7.
Ref 22 Antidepressive effect of an inward rectifier K+ channel blocker peptide, tertiapin-RQ. PLoS One. 2020 Nov 13;15(11):e0233815. doi: 10.1371/journal.pone.0233815. eCollection 2020.
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